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MONOGRAPHS    ON  EXPERIMENTAL  BIOLOGY 


THE  BIOLOGY  OF 

DEATH 


Being  a  Series  of  Lectures    Delivered    at   the    Lowell    Institute 

in  Boston  in  December  1920 


BY 

RAYMOND   PEARL 

THE   JOHNS   HOPKINS   UNIVERSITY 


PHILADELPHIA  AND  LONDON 
J.   B.   LIPPINCOTT    COMPANY 


COPYRIGHT,    1922,   BY  J.    B.  LIPPINCOTT    COMPANY 


PRINTED   BY  J.    B.   LIPPINCOTT  COMPANY 
AT  THE  WASHINGTON  SQUARE  PRESS 
PHILADELPHIA,  U.  S,  A, 


TO 

MY  WISEST  COUNSELLOR 
M.  D.  P. 


35486 


EDITOR'S  ANNOUNCEMENT 

The  rapidly  increasing  specialization  makes  it  im- 
possible for  one  author  to  cover  satisfactorily  the  whole 
field  of  modern  Biology.  This  situation,  which  exists  in 
all  the  sciences,  has  induced  English  authors  to  issue 
series  of  monographs  in  Biochemistry,  Physiology,  and 
Physics.  A  number  of  American  biologists  have  decided 
to  provide  the  same  opportunity  for  the  study  of 
Experimental  Biology. 

Biology,  which  not  long  ago  was  purely  descriptive 
and  speculative,  has  begun  to  adopt  the  methods  of  the 
exact  sciences,  recognizing  that  for  permanent  progress 
not  only  experiments  are  required  but  that  the  experi- 
ments should  be  of  a  quantitative  character.  It  will  be 
the  purpose  of  this  series  of  monographs  to  emphasize 
and  further  as  much  as  possible  this  development  of 

Biology. 

Experimental  Biology  and  General  Physiology  are  one 
and  the  same  science,  by  method  as  well  as  by  contents, 
since  both  aim  at  explaining  life  from  the  physico-chemical 
constitution  of  living  matter.  The  series  of  monographs 
on  Experimental  Biology  will  therefore  include  the  field 

of  traditional  General  Physiology. 

Jacques  Loeb, 

T.  H.  Morgan, 

W.  J.  V.  Osterhout. 


AUTHOR'S  PREFACE 

In  preparing  the  material  of  a  series  of  lectures,  given 
at  the  Lowell  Institute  in  Boston  in  December  1920,  for 
book  publication,  I  have  deemed  it  on  the  whole  best  to 
adhere  rather  closely  to  the  original  lecture  mode  of  pre- 
sentation with  all  its  informality.  Except  for  the  fact 
that  the  matter  is  here  set  fortl;i  in  somewhat  greater 
detail  than  was  possible  under  the  rigid  time  limitations 
of  the  Lowell  Institute,  and  that  the  breaking  into  chap- 
ters is  slightly  different,  the  whole  is  substantially  as  it 
was  presented  in  Boston. 

What  I  tried  to  do  in  these  lectures  was  to  bring 
together  under  a  unified  viewpoint  some  of  the  more  im- 
portant contributions  which  have  been  made  to  our  know- 
ledge of  natural  death,  from  three  widely  scattered 
sources:  namely  general  biology,  experimental  biology, 
and  statistical  and  actuarial  science.  It  will  be  obvious 
to  anyone  who  knows  the  literature  from  these  fields 
regarding  natural  death  and  the  duration  of  life  that  in 
such  an  amount  of  space  as  is  here  used,  no  one  could 
hope  to  cover  a  field  so  wide  with  anything  approaching 
completeness.  To  do  so  would  require  a  series  of  volumes 
in  place  of  one  small  one.  But  this  has  in  no  wise  been 
my  object ;  I  have  instead  hoped  that  the  very  incomplete- 
ness itself  of  this  work,  necessitated  by  my  limitations 
of  space  and  knowledge,  might  stimulate  the  reader  to 
penetrate  for  himself  further  into  the  literature  of  this 
fascinating  and  important  field  of  biology.  To  help  him 
to  start  upon  this  excursion  a  brief  bibliography  is 
appended.    It  by  no  means  completely  covers  the  field, 

but  may  perhaps  serve  as  an  introduction. 

9 


10  AUTHOR'S  PREFACE 

I  am  indebted  to  a  number  of  authors  and  publishers 
for  permission  to  use  illustrations  and  wish  here  to  ex- 
press my  great  appreciation  of  this  courtesy.  The  indi- 
vidual sources  for  these  borrowed  figures  are  in  every 
case  indicated  in  the  legends.  To  Dr.  J.  McKeen  Cattell 
I  am  especially  grateful  for  allowing  me  the  use  of  the 
blocks  from  the  magazine  publication  of  this  material  in 
the  Scientific  Monthly ;  to  Dr.  Alexis  Carrel  for  permis- 
sion to  use  unpublished  photographs  of  his  tissue  cultures ; 
and,  finally,  to  Professor  T.  H.  Morgan  for  critically 
reading    the    manuscript    and    making    many    helpful 

suggestions. 

R.  P. 

Baltimobe, 

April  19,  1922.  • 


CONTENTS 


CHAPTBR  FAQS 

I.  The  Problem 17 

II.  Conditions  op  Cellular  Immortality 51 

III.  The  Chances  of  Death 79 

rV.  The  Causes  op  Death 102 

V.  Embryology  and  Human  Mortality 138 

VI.  The  Inheritance  op  Duration  op  Lipe  in  Man  150 

VII.  Experimental  Studies  on  the  Duration  op  Lipe  186 

VIII.  Natural  Death,  Public  Health,  and  the  Population  Problem  223 

Bibliography 259 

Index 269 


ILLUSTRATIONS 

FIG.  PACK 

1.  Photograph  of  John  Shell,  claimed  to  be  131  years  old,  but  actually 

about  100,  with  his  wife  and  putative  son  (From  Nascher) 26 

2.  Showing  the  changes  in  nerve  cells  due  to  age  (From  Donaldson 

after  Hodge) 29 

3.  Paramecium,  viewed  from  the  oral  surface  (From  Jennings) 31 

4.  Diagram  showing  the  process  of  reproduction  by  fission  in  the  uni- 

cellular organism  Paramecium 32 

5.  Conjugation  in  Paramecium 32 

6.  Planaria  dorotocephala  (From  Child) 34 

7.  Beginning  of  process  of  agamic  reproduction  by  fission  in  Planaria 

(From  Child) # 35 

8.  Progress  of  agamic  reproduction  in  Stenostomum  (From  Child) ....     36 

9.  Section  across  the  posterior  part  of  an  embryo  dog-fish  (Acanthias) 

of  3.5  mm.     (From  Minot  after  Woods) 38 

10.  First  and  second  division  in  egg  of  Cyclops  (From  Child) 39 

11.  Diagram  to  show  mode  of  descent  (Modified  from  Jennings) 41 

12.  Artificially  parthenogenetic  frogs  (Loeb) 52 

13.  Piece  of  tissue  from  frog  embryo  cultivated  in  lymph  (From  Harrison)  58 

14.  Group  of  nerve  fibers  which  have  grown  from  an  isolated  piece  of 

neural  tube  of  a  chick  embryo  (From  Harrison  after  Burrows) ....     59 

15.  Human  connective  tissue  cells  fixed  and  stained  with  Giemsa  stain 

(After  Losee  and  Ebehng) 60 

16.  Pennaria  (From  Wilson) 62 

17.  Culture  of  old  strain  of  connective  tissue  (EbeUng) 63 

18.  Life  table  diagram 81 

19.  Comparing  the  expectation  of  life  in  the  17th  century  with  that  of 

the  present  time 84 

20.  Comparing  the  expectation  of  life  in  the  18th  century  with  that  of 

the  present  time 86 

21.  Comparing  the  expectation  of  life  of  ancient  Egyptians  with  that  of 

present  day  Americans 88 

22.  Comparing  the  expectation  of  life  of  ancient  Romans  with  that  of 

present  day  Americans 90 

13 


14  ILLUSTRATIONS 

TIG.  PAGE 

23.  Comparing  the  expectation  of  life  of  the  population  of  the  Roman 

provinces  Hispania  and    Lusitania    with    that  of    present    day 
Americans 91 

24.  Comparing  the  expectation  of  life  of  the  population  of  the  Roman 

provinces  in  Africa  with  that  of  present  day  Americans 92 

25.  Showing  Pearson's  results  in  fitting  the  dx  line  of  the  hfe  table  with 

5  skew  frequency  curves 95 

26.  Showing  the  relative  importance  of  the  different  organ  systems  in 

human  mortality 108 

27.  Diagram  showing  the  specific  death  rate  at  each  age  for  deaths  from 

all  causes  taken  together 116 

28.  The  specific  death  rate  at  each  age  from  breakdown  of  the  circulatory 

system,  blood  and  blood  forming  organs 118 

29.  The  specific  death  rate  at  eibh  age  from  breakdown  of  the  respira- 

tory system 120 

30.  Specific  death  rates  at  each  age  from  breakdown  of  the  primary  and 

secondary  sex  organs 125 

31.  Specific  death  rates  at  each  age  from  breakdown  of  the  kidneys  and 

related  excretory  organs 127 

32.  Specific  death  rates  at  each  age  from  breakdown  of  the  skeletal  and 

muscular  systems 128 

33.  Specific  rates  of  death  at  each  age  from  breakdown  of  the  alimentary 

tract  and  associated  organs  of  metabohsm 129 

34.  Specific  death  rates  at  each  age  from  breakdown  of  the  nervous  sys- 

tem and  sense  organs 130 

35.  Specific  death  rates  at  each  age  chargeable  against  the  skin 132 

36.  Specific  death  rates  at  each  age  from  breakdown  of  the  endocrinal 

system 133 

37.  Specific  death  rates  from  all  other  causes  of  death  not  covered  in  the 

preceding  categories 134 

38.  Percentages  of  biologically  classifiable  human  mortaUty  resulting  from 

breakdown  of  organs  developing  from  the  different  germ  layers. . .   140 

39.  Specific  death  rates  in  males  according  to  the  germ  layer  from  which 

the  organs  developed 144 

40.  Specific  death  rates  for  females 146 

41.  Survival  curves  of  members  of  the  Hyde  family  (Plotted  from  Bell's 

data) 153 


THE  BIOLOGY  OF 
DEATH 


CHAPTER  I 

THE  PROBLEM 

Probably  no  subject  so  deeply  interests  human  beings 
as  that  of  the  duration  of  human  life.  Presumably  just 
because  the  business  of  living  was  such  a  wonderfully 
interesting  and  important  one  from  the  viewpoint  of  the 
individual,  man  has  endeavored,  in  every  way  he  could 
think  of,  to  prolong  it  as  much  as  possible.  He  has  had 
recourse  to  both  natural  and  supernatural  schemes  for 
attaining  this  objective.  On  the  mundane  plane  he  has 
developed  the  sciences  and  arts  of  biolog}^  medicine  and 
hygiene,  with  the  fundamental  purpose  of  learning  the 
underlying  principles  of  vital  processes,  so  that  it  might 
ultimately  be  possible  to  stretch  the  length  of  each  indivi- 
dual's life  on  earth  to  the  greatest  attainable  degree. 
Eecognizing  pragmatically,  however,  that  at  best  the  limi- 
tations in  this  direction  were  distinctly  narrow,  when 
conceived  in  any  historical  sense,  he  has  with  singularly 
wide-spread  unanimity,  deemed  it  wise  to  seek  another 
means  of  satisfying  his  desires.  Man's  body  plainly  and 
palpably  returns  to  dust,  after  the  briefest  of  intervals, 
measured  in  terms  of  cosmic  evolution.  But,  patent  as 
this  fact  is  it  has  not  precluded  the  postulation  of  an  infin- 
ite continuation  of  that  impalpable  portion  of  man's  be- 
ing which  is  called  the  soul.    With  the  field  thus  open  we 

2  17 

1  library 
N.   C.   State    Collcire 


18  THE  BIOLOGY  OF  DEATH 

see  some  sort  of  notion  of  immortality  incorporated  in 
an  integral  part  of  almost  all  folk  philosophies  of  which 
any  record  exists. 

Now,  perhaps  unfortunately,  perhaps  fortunately,  it 
has  up  to  the  present  time  proved  impossible  absolutely 
to  demonstrate,  for  reasons  which  will  presently  appear, 
by  any  scientifically  valid  method  of  experimentation  or 
reasoning,  that  any  real  portion  of  that  totality  of  being 
which  is  an  individual  living  man  persists  after  he  dies. 
Equally,  for  the  same  reasons,  science  cannot  absolutely 
demonstrate  that  such  persistence  does  not  occur.  The 
latter  fact  has  had  two  important  consequences.  In  the  first 
place,  it  has  permitted  man}^  millions  of  people  to  derive 
a  real  comfort  of  soul  in  sorrow,  and  a  fairly  abiding  tran- 
quility of  mind  in  general  from  the  belief  that  immortality 
is  a  reality.  Even  the  most  cynical  of  scoffers  can  find  lit- 
tle fault  with  such  a  result,  the  world  and  human  nature 
being  constituted  as  they  are.  The  other  consequence  of 
science's  present  inability  to  lay  bare,  in  final  and  irre- 
fragable terms,  the  truth  about  the  course,  if  any,  of 
events  subsequent  to  death  is  more  serious.  It  opens  the 
way  for  recurring  mental  epidemics  of  that  intimate  mix- 
ture of  hyper-credulity,  hyper-knavery,  and  mysticism, 
which  used  to  be  called  spiritualism,  but  now  usually  pre- 
fers more  seductive  titles.  We  are  at  the  moment  in  the 
midst  of  perhaps  the  most  violent  and  destructive  epi- 
demic of  this  sort  wliich  has  ever  occurred.  Its  evil  lies  in 
the  fact  that  in  exact  proportion  to  its  virulence  it  des- 
troys the  confidence  of  the  collective  mind  of  humanity 
in  the  enduring  efficacy  of  the  only  thing  wliich  the  history 
of  mankind  has  demonstrated  to  contribute  to  the  real 
advancement  of  his  intellectual,  physical,  spiritual  and 
moral  well  being,  namely  that  orderly  progression  of 
ascertained  knowledge  which  we  now  call  science. 


THE  PROBLEM  19 

The  reason  why  science  finds  itself  helpless  to  pre- 
vent spiritualism's  insidious  sapping  of  the  intellectual 
fiber  of  the  race  is  because  it  is  asked  to  prove  a  negative, 
upon  the  basis  of  unreal  data.  How  difficult  such  a  task 
is  is  obvious  as  it  is  proverbial.  Until  science  has  demon- 
strated that  there  is  not  a  continuation  of  individual 
supernatural  existence  after  natural  death,  the  spiritual- 
ist can,  and  will,  come  forward  with  supposed  demonstra- 
tions that  there  is  such  a  continuation.  But  the  most 
characteristic  feature  of  science  is  its  actuality,  its  reality, 
its  naturality.  Pearson  has  pointed  out,  in  characteristi- 
cally clear  and  vigorous  language,  the  reason  why,  in  the 
minds  of  uninformed  persons,  science  appears  helpless  in 
this  situation.    He  says: 

Scientific  ignorance  may  either  arise  from  an  insuflficient  classification 
of  facts,  or  be  due  to  the  unreality  of  the  facts  with  which  science  has  been 
called  upon  to  deal.  Let  us  take,  for  example,  fields  of  thought  which 
were  very  prominent  in  medieval  times,  such  as  alchemy,  astrology,  witch- 
craft. In  the  fifteenth  century  nobody  doubted  the  "facts"  of  astrology 
and  witchcraft.  Men  were  ignorant  as  to  how  the  stars  exerted  their 
influence  for  good  or  ill;  they  did  not  know  the  exact  mechanical  process 
by  which  all  the  milk  in  a  village  was  turned  blue  by  a  witch.  But  for 
them  it  was  nevertheless  a  fact  that  the  stars  did  influence  human  lives, 
and  a  fact  that  the  witch  had  the  power  of  turning  the  milk  blue.  Have 
we  solved  the  problems  of  astrology  and  witchcraft  today? 

Do  we  now  know  how  the  stars  influence  human  lives,  or  how  witches 
turn  milk  blue?  Not  in  the  least.  We  have  learnt  to  look  upon  the  facts 
themselves  as  unreal,  as  vain  imaginings  of  the  untrained  human  mind; 
we  have  learnt  that  they  could  not  be  described  scientifically  because  they 
involved  notions  which  were  in  themselves  contradictory  and  absurd.  With 
alchemy  the  case  was  somewhat  difi"erent.  Here  a  false  classification  of 
real  facts  was  combined  with  inconsistent  sequences — that  is,  sequences 
not  deduced  by  a  rational  method.  So  soon  as  science  entered  the  field 
of  alchemy  with  a  true  classification  and  a  true  method,  alchemy  was  con- 
verted into  chemistry  and  became  an  important  branch  of  human  knowl- 
edge. Now  it  will,  I  think,  be  found  that  the  fields  of  inquiry,  where 
science   has   not   yet   penetrated   and   where    the    scientist    still    confesses 


20  THE  BIOLOGY  OF  DEATH 

ignorance,  are  very  like  alchemy,  astrology,  and  witchcraft  of  the  Middle 
Ages.  Either  they  involve  facts  which  are  in  themselves  unreal — con- 
ceptions which  are  self-contradictory  and  absurd,  and  therefore  incapable 
of  analysis  by  the  scientific  or  any  other  method — or,  on  the  other  hand, 
our  ignorance  arises  from  an  inadequate  classification  and  a  neglect  of 
scientific  method. 

This  is  the  actual  state  of  the  case  with  those  mental  and  spiritual 
phenomena  which  are  said  to  lie  outside  the  proper  scope  of  science,  or 
which  appear  to  be  disregarded  by  scientific  men.  No  better  example 
can  be  taken  than  the  range  of  phenomena  which  are  entitled  Spiritualism. 
Here  science  is  asked  to  axxalyse  a  series  of  facts  which  are  to  a  great  extent 
unreal,  which  arise  from  the  vain  imaginings  of  untrained  minds  and 
from  atavistic  tendencies  to  superstition.  So  far  as  the  facts  are  of  this 
character,  no  account  can  be  given  of  them,  because,  like  the  witch's 
supernatural  capacity,  their  unreality  will  be  found  at  bottom  to  make 
them  self-contradictory.  Combined,  however,  with  the  unreal  series  of 
facts  are  probably  others,  connected  with  hypnotic  and  other  conditions, 
which  are  real  and  only  incomprehensible  because  there  is  as  yet  scarcely 
any  intelligent  classification  or  true  application  of  scientific  method.  The 
former  class  of  facts  will,  like  astrology,  never  be  reduced  to  law,  but  will 
one  day  be  recognized  as  absurd;  the  other,  like  alchemy,  may  grow  step 
by  step  into  an  important  branch  of  science.  Whenever,  therefore,  we 
are  tempted  to  desert  the  scientific  method  of  seeking  truth,  whenever  the 
silence  of  science  suggests  that  some  other  gateway  must  be  sought  to 
knowledge,  let  us  inquire  first  whether  the  elements  of  the  problem,  of 
whose  solution  we  are  ignorant,  may  not  after  all,  like  the  facts  of  witch- 
craft, arise  from  a  superstition,  and  be  self-contradictory  and  incompre- 
hensible because  they  are  unreal. 

Let  US  recapitulate  briefly  our  discussion  to  this  point. 
Mankind  has  endeavored  to  prolong  the  individual  life  by 
natural  and  by  supernatural  means.  This  latter  plan 
falls  outside  the  present  purview  of  the  scientific  method. 
The  former  is,  in  last  analysis,  responsible  for  a  consid- 
erable part,  at  least,  of  the  development  of  the  science 
of  biology,  pure  and  applied,  and  the  arts  which  found 
their  operations  upon  it.  Biology  can  and  has  contributed 
much  to  our  knowledge  of  natural  death  and  the  causes 
which  determine  the  duration  of  life.  It  is  the  purpose 
of  this  book  to  review  some  of  the  more  important  aspects 


THE  PROBLEM  21 

of  this  phase  of  biological  science,  and  endeavor  to  set 
forth  in  an  orderly  and  consistent  manner  the  jjresent 
state  of  knowledge  of  the  subject. 

The  problem  of  natural  death  has  two  aspects,  one 
general,  the  other  special.  These  may  be  stated  in 
this  way : 

1.  Why  do  living  things  die?  Wliat  is  the  meaning 
of  death  in  the  general  philosophy  of  biolog}^  ? 

2.  Why  do  living  things  die  ivhen  they  do?  What 
factors  determine  the  duration  of  life  in  general  and  in 
particular,  and  what  is  the  relative  influence  of  each  of 
these  factors  in  producing  the  observed  result? 

Both  of  these  problems  have  been  the  subject  of  much 
speculation  and  discussion.  There  has  accumulated, 
especially  in  recent  years,  a  considerable  amount  of  new 
experimental  and  statistical  data  bearing  upon  them.  I 
hope  to  be  able  in  what  follows  to  show  that  this  new 
material,  together  with  that  which  has  for  a  long  time 
been  a  part  of  the  common  store  of  biological  knowledge, 
makes  possible  a  clearer  and  more  logically  consistent 
picture  than  we  have  had  of  the  meaning  of  death  and 
the  determination  of  longevity.  Let  us  first  examine  in 
brief  review  the  broad  generalizations  about  death  which 
have  grown  up  in  the  course  of  the  development  of  biolog}% 
and  which  may  now  be  regarded  as  agreed  to  by  practi- 
cally all  biologists. 

BIOLOGICAL   GENERALIZATIONS    ABOUT    NATURAL   DEATH 

The  significant  general  facts  which  are  known  about 
natural  death  are  these; 

(A).  There  is  an  enormous  variation  in  the  duration 
of  life,  both  intra  and  inter-racially.  Table  I,  which  is 
adapted  from  various  authorities,  is  to  be  read  with  the 


22 


THE  BIOLOGY  OF  DEATH 


understanding  that  the  figures  are  estimates,  frequently 
based  upon  somewhat  general  and  inexact  evidence,  and 
record  extreme,  though  it  is  believed  authentic  instances. 
While  the  figures,  on  the  accounts  which  have  been  men- 
tioned, are  subject  to  large  probable  errors,  the  table  does 
give  a  sufficiently  reliable  general  picture  of  the  truth 
to  indicate  the  enormous  differences  which  exist  among 
different  forms  of  animal  life  in  respect  of  longevity. 

TABLE  1 

Longevity  of  Animals 


Animal 


Lower  invertebrates 

Insects 

Fish 

Ampliibia 

Reptiles 

Birds 

Mammals 


Approximate  limits  of  maximum  duration 
of  life  in  different  species 


Under  100  hours  to  ? 

Under  100  hours  to  17  years 

?  to  267  years 

?  to    36  years 

?  to  175  years 

9  years  to  118  years 

1}4  years  to  over  100  years 


We  see  from  tliis  table  that  life  may  endure  in  differ- 
ent forms  from  only  the  briefest  period,  measured  in 
hours  as  in  the  case  of  Ephemeridae,  to  somewhere  in 
the  hundreds  of  years.  The  extremely  long  durations 
are  of  course  to  be  looked  upon  with  caution  and  reserva- 
tion, but  if  we  accept  only  extreme  cases  of  known  dura- 
tion of  life  in  man,  the  range  of  variation  in  this 
characteristic  of  living  tilings  is  sufficiently  wide. 

It  is  probable  that  man,  in  exceptional  instances,  is 
nearly  the  longest  lived  of  all  mammals.  The  common 
idea  that  whales  and  elephants  attain  great  longevity 
appears  to  be  not  well  founded.  The  absolutely  authentic 
instances  of  human  survival  beyond  a  century  are,  con- 
trary to  the  prevalent  view  and  customary  statistics, 
extremely   rare.     The  most  painstaking   and   accurate 


THE  PROBLEM  23 

investigation  of  the  frequency  of  occurrence  of  centen- 
arians which  has  ever  been  made  is  that  of  T.  E.  Young. 
Because  of  the  considerable  intrinsic  interest  of  the 
matter,  and  the  popular  misconceptions  which  generally 
prevail  about  it,  it  will  be  worth  while  to  take  a  little 
time  to  examine  Young's  methods  and  results.  He  points 
out  in  the  beginning  that  the  evidence  of  great  age  which 
is  usually  accepted  by  census  officials,  by  registrars  of 
death,  by  newspaper  reporters,  and  by  the  general  public, 
is,  generally  speaking,  of  no  validity  or  trustworthiness 
whatever.  Statements  of  the  person  concerned,  or  of  that 
person's  relatives  or  friends,  as  to  extreme  longevity, 
can  almost  invariably  be  shown  by  even  a  little  investiga- 
tion to  be  extremely  unreliable.  To  be  acceptable  as 
scientific  evidence  any  statement  of  great  age  must  be 
supported  by  unimpeachable  documentary  proof  of  at 
least  the  following  points: 

a.  The  date  of  hirth^  or  of  baptism. 

b.  The  date  of  death. 

c.  The  identity  of  the  person  dying  at  a  supposed  very  advanced  age 

with  the  person  for  whom  the  birth  or  baptismal  record,  upon 
which  the  claim  of  great  age  is  based,  was  made  out. 

d.  In  the  case  particularly  of  married  women  the  date  of  marriage, 

the  person  to  whom  married,  and  any  other  data  which  will 
help  to  establish  proof  of  identity. 

In  presumptive  cases  of  great  longevity,  wliich  on 
other  grounds  are  worthy  of  serious  consideration,  it  is 
usually  in  respect  of  item  c — the  proof  of  identity — that 
the  evidence  is  weakest.  Every  student  of  genealogical 
data  knows  how  easy  it  is  for  the  f ollomng  sort  of  thing 
to  happen.  John  Smith  was  born  in  the  latter  half  of 
the  eighteenth  century.  His  baptism  was  duly  and  pro- 
perly registered.     He  unfortunately  died  at  the  age  of 


24  BIOLOGY  OF  DEATH 

say  15.  By  an  oversight  his  death  was  not  registered. 
In  the  same  year  that  he  died  another  male  child  was 
born  to  the  same  parents,  and  given  the  name  of  John 
Smith,  in  commemoration  perhaps  of  his  deceased  brother. 
This  second  John  Smith  was  never  baptized.  He  at- 
tained the  age  of  85  years,  and  then  because  of  the  appear- 
ance of  extreme  senility  which  he  presented,  his  stated  age 
increased  by  leaps  and  bounds.  A  study  of  the  baptismal 
records  of  the  town  disclosed  the  apparent  fact  that  he 
was  just  100  years  old.  The  case  goes  out  to  the  public 
as  an  unusually  well  authenticated  case  of  centenarianism, 
when  of  course  it  is  nothing  of  the  sort. 

Young  applies  vigorously  the  criteria  above  enumer- 
ated first,  to  the  historically  recorded  cases  of  great  long- 
evity such  as  Thomas  Parr,  et  id  genus  omne,  and  rejects 
them  all;  and  second  to  the  total  mortality  experience 
of  all  the  Life  Assurance  and  Annuity  Societies  of  Great 
Britain  and  the  aim.uity  experience  of  the  National  Debt 
Office.  The  number  of  persons  included  in  the  experience 
was  close  upon  a  million.  He  found  in  this  material,  and 
from  other  outside  e\^dence,  exactly  30  persons  who  lived 
100  or  more  years.  In  Table  2  the  detailed  results  of 
his  inquiry  are  shown  in  condensed  form. 

It  will  be  noted  from  this  table  that  the  most  extreme 
case  of  longevity  which  Young  was  able  to  authenticate 
was  about  a  month  and  a  half  short  of  111  years.  Of 
the  30  centenarians  recorded  21  were  women  and  9  were 
men.  The  superiority  of  women  in  expectation  of  life  is 
strikingly  apparent  at  the  very  high  age  of  100  years.  We 
shall  later  see  that  tliis  is  merely  a  particularly  noteworthy 
instance  of  a  phenomenon  which  is  common  to  a  great 
portion  of  the  life  span. 


Library 
N.   C.   State   College 


THE  PROBLEM 


25 


The  contrast  between  these  proved  findings  of  Young, 
exceedingly  modest  both  in  respect  of  numbers,  and  ex- 
tremity of  longe\dty,  and  the  loose  data  on  centenarianism 

TABLE  2 

Authentic  Instances  of  Centenarianism  {from  Young) 


Age  at  death 

Social  status 

(or  living) 

Sex 

(single  or 
married) 

tJX^Jk 

Years 

Mouths 

Days 

9 

M 

110 

321 

9 

M 

108 

,    , 

144 

9 

M 

105 

8 

. .  . 

9 

S 

104 

9 

16 

9 

M 

103 

9 

28 

9 

? 

103 

•  • 

269 

9 

M 

103 

3 

7 

cf 

? 

103 

1 

8 

& 

? 

102 

9 

2 

9 

? 

102 

,   , 

218 

9 

S 

102 

2 

10 

9 

S 

102 

1 

8 

9 

s 

102 

•  • 

21 

9* 

s 

102 

•   • 

19 

cT 

? 

102 

,    . 

2 

9t 

s 

101 

10 

4 

9 

s 

101 

8 

25 

d' 

? 

101 

,    , 

263 

cf 

? 

101 

4 

. .  ■ 

9 

s 

101 

1 

16 

9 

s 

101 

1 

4 

cT 

? 

101 

,  , 

32 

9 

s 

101 

,   , 

1 

& 

? 

100 

9 

4 

9 

s 

100 

7 

6 

9 

s 

100 

6 

9 

9 

M 

100 

•  • 

133 

& 

M 

100 

2 

24 

9 

s 

ino 

1 

10 

cT 

? 

100 

20 

♦  Living  30  September,  1905. 
t  Living  31  July,  1898. 

which  one  can  find  in  any  year's  mortality  statistics,  is 
striking.  In  an  examination  of  the  matter  recently,  for 
example,  it  was  found  that  in  the  registration  area  of  the 


26  BIOLOGY  OF  DEATH 

United  States  there  were  recorded  in  the  year  1916,  out 
of  a  total  of  1,001,921  deaths  at  all  ages  the  following  as 
of  ages  100  or  over: 

White    males     137 

Colored  males    116 

White  females   180 

Colored    females    216 

Total    649 

In  this  large  total  4  persons  were  recorded  as  ha\dng 
died  at  the  age  of  120,  and  one,  a  colored  female,  at  the 
preposterous  age  of  134! 

B.  There  is  no  generally  valid,  orderly  relationship 
hetiveen  the  average  duration  of  life  of  the  individuals 
composing  a  species  and  any  other  hroad  fact  now  known 
in  their  life  history,  or  their  structure,  or  their  physiology. 
Many  attempts  have  been  made  to  set  up  generalizations 
establishing  connections  of  this  sort.  Weismann  particu- 
larly, has  endeavored  to  establish  such  relations  only  to 
have  them  overthro^vn,  sometimes  by  facts  which  he  him- 
self presents.  It  has,  for  example,  been  contended  that  the 
larger  an  animal  the  longer  its  life.  This  is  obviously 
no  general  law.  Again  it  has  been  held  that  no  animal 
lives  after  reproducing,  except  such  as  care  for  their 
young,  but  almost  numberless  instances  can  be  adduced 
where  no  such  relationship  holds.  It  will  not  pay  to  ex- 
amine all  the  hypotheses  of  this  general  type  which  have, 
at  one  time  or  another,  been  put  forward.  With  one  excep- 
tion, to  which  we  shall  advert  immediately,  they  all  suffer 
from  too  many  important  exceptions  to  be  considered 
valid  generalizations. 

C.  Natural  death  as  distinguished  from  accidental 
death  is  preceded  hy  definite  structural  and  functional 


Fig.   1.      Photograph  of    John  SheU,  claimed  to  be  131  years  old,  but  act- 
ually  about  100,  with  hie  wife  and  putative  son.         (From  Nascher). 


THE  PROBLEM  27 

changes  in  the  body.  These  changes  in  the  structure  of 
different  organs  and  parts  of  the  body,  and  in  their  man- 
ner of  functioning  constitute  the  material  basis  of  what  is 
called  senescence  or  growing  old.  Some  of  the  morpho- 
logical and  physiological  changes  which  cliaracterize  ex- 
treme senescence  are  apparent  and  known  to  all.  Such 
are  in  case  of  man  the  bent  posture  which  means  an  altered 
position  and  fusion  of  the  elements  of  the  vertebral 
column,  the  wrinkled  visage,  which  denotes  a  profound  al- 
teration of  tissue  elements,  and  the  shuffling  and  uncer- 
tain gait,  which  bespeaks  a  failing  motor  coordination. 
In  Figure  1  these  senescent  changes  are  all  well  indicated 
in  the  case  of  an  old  man  who  has  received  much  news- 
paper notice,  ** Uncle''  John  Shell  of  Kentucky,  who  is 
here  sIiowtl  with  his  last  wife  and  supposed  son.  This 
poor  old  man  has  been  exliibited  about  that  part  of  the 
country  as  ''the  oldest  living  human  being,''  at  a  claimed 
age  of  131  years.  As  a  matter  of  fact,  Nascher,  who  has 
made  a  careful  investigation  of  the  case,  finds  him  to  be 
''about  one  hundred  years  old,  possibly  a  year  younger 
or  older. ' '  The  paternity  of  the  4V2  year  old  boy,  though 
claimed  by  Shell,  is  in  considerable  doubt. 

Beside  these  obvious  senescent  changes  there  are 
going  on  even  more  significant  changes  in  the  cellular  ele- 
ments which  compose  the  body.  Certain  of  these  cellular 
changes  of  age  were  described  in  a  series  of  Lowell  lec- 
tures given  a  little  more  than  a  decade  ago  by  the  late 
Dr.  Charles  Sedgwick  Minot.  Over  a  quarter  of  a  cen- 
tury ago  Hodge  made  a  careful  study  of  senile  changes  in 
nerye  cells.  In  a  man  dying  naturally  at  92  years  of  age 
he  found  marked  changes  in  the  cells  of  the  spinal  gangha 
as  compared  with  those  of  a  new  born  babe.  The  chief 
differences  are  exhibited  in  Table  3. 


28 


BIOLOGY  OF  DEATH 


TABLE  3 

Showing  the  Principal  Differences  Observed  on  Comparing  the  Spinal  Ganglion 
Cells  (First  Cervical  Ganglion)  from  a  Child  at  Birth  With  Those 
from  a  Man  Dying  of  Old  Age  at  Ninety-two  Years. 
(From  Hodge's  data) 


Baby  at  birth.    Male 

Old  Man 

Volume  of  nucleus 
Nucleoli  visible 
Deep  pigmentation 
Slight  pigmentation 

100  per  cent. 

53  per  cent. 

0  per  cent. 

0  per  cent. 

64.2  per  cent. 

5     per  cent. 

67     per  cent. 

33     per  cent. 

Hodge  found  still  more  marked  changes  in  the  anten- 
nary  lobe  of  the  nervous  system  of  the  honey  bee.  The 
nature  of  the  changes  is  shown  in  Figure  2. 

In  the  ganglion  cells  of  both  man  and  the  honey  bee, 
the  volume  of  the  nucleus  in  proportion  to  that  of  the 
rest  of  the  cell  body  becomes  reduced  with  advancing  age. 
Minot  showed  that  this  was  a  very  general  phenomenon 
in  senescence,  and  was  a  continuous  process  from  birth  to 
death.  He  gave  to  it  and  related  and  associated  cellular 
changes  the  name  "cytomorphosis,"  and  attributed  to  it 
the  greatest  significance  in  bringing  about  senescence  and 
death.  As  we  shall  presently  see,  cytomorphosis  may 
perhaps  more  justly  be  regarded  as  one  of  the  morpho- 
logical results  of  senescence  rather  than  its  cause. 

Eecently  Mrs.  Pixell-Goodrich,  an  English  worker,  has 
re-studied  the  senescent  changes  in  the  cells  of  the  honey 
bee.  Her  work  shows  in  a  striking  way  the  loss  of  proto- 
plasm in  the  aged  cell.  In  the  young  bee  immediately 
after  hatching,  the  cells  are  large  and  plump,  only  separ- 
ated from  each  other  by  narrow  strands  of  connective 
tissue.  In  the  same  region  of  the  same  ganglion  in  an  old 
bee  which  came  from  a  liive  on  a  fine  day  in  March,  but 
was  too  weak  to  effect  a  cleansing  flight  and  soon  became 
moribund,  the  nerve  cells  were  quite  worn  out.     There 


THE  PROBLEM 


29 


was  left  only  a  framework  of  connecting  tissue,  with  an 
occasional  nucleus  of  a  nerve  cell  in  a  more  or  less 
necrotic  condition,  with  only  a  little  cytoplasm  around  it. 


fi. 


Fig.  2. — Showing  the  changes  in  nerve  cells  due  to  age.  1,  spinal  ganglion  cells  of  a  still- 
born male  child;  2,  spinal  ganglion  cells  of  a  man  dying  at  ninety-two  years;  N.  nuclei. 
In  the  old  man  the  cytoplasm  is  pigmented,  the  nucleus  is  small,  and  the  nucleolus  much 
shrunken  or  absent.  Both  sections  taken  from  the  first  cer\'ical  ganglion,  X  250 
diameters;  3,  nerve  cells  from  the  antennary  ganglion  of  a  honey-bee,  just  emerged  in  the 
perfect  form;  4,  cells  from  the  same  locality  of  an  aged  honey-bee.  In  3,  the  large 
nucleus  (black)  is  surrounded  by  a  thin  layer  of  cytoplasm.  In  4,  the  nucleus  is  stellate, 
and  the  cell  substance  contains  large  vacuoles  with  shreds  of  cytoplasm.  (From  Donaldson 
after  Hodge). 

There  are  other  and  perhaps  even  more  general  and 
striking  morphological  changes  in  senescence  than  the 
changed  relation  between  cytoplasm  and  nucleus. 
Conklin  says : 

By  all  odds  the  most  important  structural  peculiarity  of  senescence  is 
the  increase  of  metaplasm  or  differentiation  products  at  the  expense  of 
the  general  protoplasm.  This  change  of  general  protoplasm  into  products 
of  differentiation  and  of  metabolism  is  an  essential  feature  of  embryonic 
differentiation  and  it  continues  in  many  types  of  cells  until  the  entire 
cell  is  almost  filled  with   such  products.     Since  nuclei   depend   upon   the 


30  BIOLOGY  OF  DEATH 

general  protoplasm  for  their  growth,  they  also  become  small  in  such 
cells.  If  this  process  of  the  transformation  of  protoplasm  into  differentia- 
tion products  continues  long  enough  it  necessarily  leads  to  the  death  of 
the  cell,  since  the  continued  life  of  the  cell  depends  upon  the  interaction 
between  the  general  protoplasm  and  the  nucleus.  In  cells  laden  with  the 
products  of  differentiation,  the  power  of  regulation  is  first  lost,  then  the 
power  of  division,  and  finally  the  power  of  assimilation;  and  this  is 
normally  followed  by  the  senescence  and  death  of  the  cells. 

D.  Natural  death  {as  distinguished  from  accidents) 
occurs  normally  and  necessarily  only  in  animals  com- 
posed of  many  cells.  Unicellular  organisms  are  finally 
kno^vn,  to  a  considerable  extent  as  the  result  of  the  bril- 
liant and  painstaking  researches  of  Woodruff  and  his 
students,  to  be  immortal  in  esse  as  well  as  in  posse.  Since 
the  discovery  by  Woodruff  and  Erdman  of  the  process 
of  nuclear  reorganization,  which  they  call  endomixis,  this 
conclusion  is  as  solidly  grounded  if  we  regard  a  cycle  of 
protozoan  divisions  as  the  homologue  of  the  metazoan 
body,  as  it  is  if  we  consider  each  individual  protozoan  as 
such  homologue.  Woodruff  has  been  cultivating  the  com- 
mon unicellular  form  Paramecium,  sho^\Ti  in  Figure  3, 
for  over  13  3^ears. 

During  all  this  time  no  conjugation  or  pairing  of  in- 
dividuals has  occurred.  In  a  recent  letter  Dr.  Woodruff 
says:  ** After  we  had  discovered  and  worked  out  endo- 
mixis there  seemed  no  particular  use  of  carefully  record- 
ing the  number  of  generations  each  day.  But  the  culture 
is  still  going  on  as  well  as  ever  and  is  at  approximately 
the  8500th  generation — 13^/2  years  old!  On  May  1, 
1915,  (just  8  years  old)  it  was  at  the  5071st  generation." 
If  in  8500  generations — a  duration  of  healthy  reproduc- 
tive existence  which,  if  the  generation  were  of  the  same 
length  as  in  man  would  represent  roughly  a  quarter  of  a 
million  years  in  absolute  time — natural  death  has  not 


THE  PROBLEM 


31 


occurred,  we  may  with  reasonable  assurance  conclude 
that  this  animal  is  immortal. 

Of   even  more   probative  value,   in  the   opinion   of 
some  workers,   than   the   results    on   Paramecium    are 


Fig.  3. — Paramecium,  viewed  fron  the  oral  surface.  L.  left  side;  R,  right  side;  an.,  anua; 
ec,  ectosarc;  e/i.,  endosarc;/.  ».,  food  vacuoles;  &,  gullet;  m,  mouth;  via.,  macronucleus;  mi., 
micronucleus;  o.  g.,  oral  groove;  P.,  pellicle;  tr.,  trichocyst  layer.  The  arrows  show  the 
direction  of  movement  of  the  food  vacuoles.     (From  Jennings). 

the   recent  experiments   of   Hartmann,   who   cultivated 
Eudorina  elegans  for  over  600  generations  without  con- 
jugation or  any  nuclear  reorganization  corresponding  to 
endomixis,  and  no  depression  in  the  culture  occurred. 
The  distinction  between  Protozoa  and  Metazoa  in 


32  BIOLOGY  OF  DEATH 

respect  of  the  incidence  of  natural  death  is  so  important 
that  it  requires  a  somewhat  detailed  explanation,  together 
with  the  reasons  for  it.  Protozoa  reproduce  by  a  process 
of  simple  division  or  fission.  A  particular  individual 
after  growing  to  a  certain  size  simply  divides  transversely 
into  two  like  individuals,  at  first  smaller  in  size,  but  ra- 


/    \ 


/ 


\ 


Fig.  4 — Diagram  showing  the  process  of  reproduction  by  Fig.  5 — Conjugation 

fission  in  the  unicellular  orginism  Paramecium.  in  Paramecium. 

pidly  growing  to  full  adult  magnitude.  The  essential 
gross  features  of  this  process  are  illustrated  in  Figure  4. 
One  cannot  say,  after  the  act  of  fission  is  accomplished, 
which  is  parent  and  which  is  offspring.  One  individual 
simply  becomes  two  and,  in  the  process  of  becoming  two, 
loses  totally  its  own  identity  as  an  individual.  Upon  occa- 
sion another  process  kno^^ni  as  conjugation  may  intervene. 
In  this  process  two  individuals  mate  together.  By  a 
process  of  assortative  mating,  like  sizes  pair  together, 


THE  PROBLEM  33 

as  was  first  shown  by  the  writer  and  later  confirmed  by 
Jennings.  After  pairing  has  occurred  an  interchange  of 
nuclear  substance  occurs  by  a  mechanism  described  and 
figured  in  many  elementary  textbooks  of  zoology.  This 
process  of  conjugation  need  not  further  concern  us  here, 
for  the  reason  that  Woodruff,  in  the  work  already  referred 
to,  has  shown  that  this  phenomenon  is  not  essential  to 
the  continued  life  of  the  race.  Its  place  may  be,  and 
normally  very  frequently  is,  taken  by  the  process  called 
endomixis.  In  this  process  there  occurs  a  nuclear  break- 
down and  reorganization  which  appears  to  be  the  equiva- 
lent, functionally  at  least,  of  that  which  takes  place 
during  conjugation. 

There  has  been  much  discussion,  particularly  among 
European  workers,  as  for  example  Doflein,  Jollos,  Wede- 
kind,  Slotopowski,  and  others,  about  certain  philosophi- 
cal, not  to  say  metaphysical,  aspects  of  immortality  in 
the  Protozoa.  But  all  such  discussion  has  in  no  wise  dis- 
turbed or  altered  the  plain  physical  fact  that  there  is  no 
place  for  death  in  a  scheme  of  reproduction  by  simple 
fission,  such  as  is  illustrated  in  Figure  4.  Notliing  is  left 
at  any  stage  to  fulfill  the  proverbial  scheme  of  '^dust  to 
dust  and  ashes  to  ashes. ' '  When  an  individual  is  throuGrh 
its  single  indi\ddual  existence  it  simply  becomes  two  indi- 
viduals, wliich  go  on  playing  the  fascinating  game  of 
living  here  and  now. 

In  a  few  of  the  simplest  and  most  lowly  organized 
groups  of  many-celled  animals  or  Metazoa  tliis  power  of 
multiplication  by  simple  fission,  or  budding  off  a  portion 
of  the  body  which  reproduces  the  whole,  is  retained  as 
a  facultative  asset.  This  process  of  reproduction  in  which 
the  somatic  or  body  cells  of  one  generation  produce  the 
somatic  cells  of  the  next  generation  has  been  called 
agamic  reproduction.  It  occurs  as  the  more  usual  but  not 

3 


34 


BIOLOGY  OF  DEATH 


n^-v/ 


M 


m 


H 


'3tt;« 


I 


m 


r,o.  e.-P.an.ri.do,otocephala:  - -- Vl''cSr<5! ^  "''  "«--""^''"'^  "'•  ''"™"' 


THE  PROBLEM 


35 


exclusive  mode  of  reproduction,  in  some  or  all  forms  of 
the  three  lowest  groups  of  multicellular  organisms,  the 
sponges,  flatworms,  and  coelenterates.  More  rarely  it 
may  occur  in  other  of  the  lower  invertebrate 
groups.  It  may  occur  in  the  f  orai  of  budding 
or  of  fission  comparable  to  that  of  the  Proto- 
zoa, The  agamic  reproduction  of  one  of  the 
flatworms,  Planaria  dorotoceiyJiala,  studied 
by  the  writer  many  years  ago,  as  shown  in 
Figure  6,  may  serve  as  an  illustration. 

This  simply  organized  worm,  which  lives 
under  stones  in  sluggish  streams  and  ponds, 
after  attaining  a  certain  size,  mil  under  the 
appropriate  environmental  conditions  exhibit 
a  constriction  tov^ards  the  posterior  end  of 
the  body,  as  shown  in  Figure  7. 

For  a  time  the  animal  moves  about  as  a 
rather  ungainly  double  individual.  It  finally 
separates  into  two.  The  larger  anterior  part 
forms  a  new  tail,  and  the  smaller  posterior 
fission  product  forms  a  new  head  and  rapidly 
grows  to  full  size.  The  process  is,  in  princi- 
ple, exactly  the  same  as  the  multiplication  of 
Paramecium  by  fission.  In  another  member 
of  the  same  general  group  of  animals  as 
Planaria,  named  Stenostomum,  several  fis- 
sion planes  may  form  and  the  process  start 
anew  before  the  products  delimited  by  the 
first  plane  have  separated.  As  a  result,  we 
get  frequently  in  this  form  chains  of  indi\'id- 
uals  attached  in  a  long  string  to  each  other, 
as  shown  in  Figure  8. 

It  is  obvious  that  so  long  as  reproduction  goes  on  in 


Fig. — 7.  Begin- 
ning of  process  of 
agamic  repro- 
d  u  c  t  i  o  n  by  fis- 
sion in  planaria. 
(From  Child) 


36 


BIOLOGY  OF  DEATH 


/. 


2. 


I.I. 


1.2. 


2. 


38 


/N 


I.I.I. 


1. 1.2. 


1.2. 


2.1. 


2.2. 


I.I.I. 


1. 1.2. 


2. I. I. 


2  'I  '*^ ' 


2.2. 


40 


Fig  8-Progre8S  of  agamic  reproduction  in  Stenostomum :  the  sequence  in  the  formation  of  new 
**  ^  zooida  is  indicated  by  the  numerals.  (From  Child.). 


THE  PROBLEM  37 

this  manner  in  these  multicellular  forms  there  is  no  place 
for  death.  In  the  passage  from  one  generation  to  the 
next  no  residue  is  left  beliind.  Agamic  reproduction  and 
its  associated  absence  of  death  occurs  very  commonly  in 
plants.  Budding  and  propagation  by  cuttings  are  the 
common  forms  in  which  it  is  seen.  The  somatic  cells  have 
the  capacity  of  continuing  multiplication  and  life  for  an 
indefinite  duration  of  time,  so  long  as  they  are  not  acci- 
dentally caught  in  the  breakdoAvn  and  death  of  the  whole 
individual  in  which  they  are  at  the  moment  located.  Thus 
virtually  every  apple  tree  in  every  orchard  in  this  coun- 
try is  simply  a  developed  branch  or  bud  of  some  original 
apple  tree  from  which  it  was  cut,  in  many  cases  centuries 
ago.  Apple  trees  cannot  of  their  own  unaided  efforts 
propagate  either  buds  or  cuttings.  So,  until  the  interven- 
tion of  man,  some  apple  trees  died  natural  deaths,  somati- 
cally speaking,  just  as  do  the  higher  animals  of  which 
we  shall  speak  presently.  But  their  cells  were  inherently 
capable  of  better  things,  as  was  demonstrated  when  man 
first  cut  off  a  shoot  from  an  old  apple  tree  and  provided 
it  with  a  root  by  grafting.*  Then  it  went  on  and  made  a 
new  tree.  From  it  in  turn  cuttings  were  taken,  and  so  the 
process  has  continued  to  the  present  day.  A  part  of  the 
soma  of  one  generation  produces  the  soma  of  the  next 
generation  and  goes  on  living  indefinitely. 

A  different  mode  of  reproduction  is  characteristic 
of  higher  multicellular  animals,  and  in  all  but  the  lowest 
groups  is  the  exclusive  method.  A  new  individual  is 
started  by  the  union  of  two  peculiar  cells  of  extraordinary 
potentialities,  called  germ  cells.  These  germ  cells  are  of 
two  sorts,  ova  and  spermatozoa.    In  bisexual  organisms 


*  This  provision  of  roots  was  not  essential,  only  practically  convenient. 
The  cutting  would,  if  enough  pains  were  taken,  grow  its  own  roots. 


38 


BIOLOGY  OF  DEATH 


the  former  are  borne  in  the  female,  and  the  latter  in  the 
male  body.  Both  sorts  undergo  a  complicated  prepara- 
tion for  union,  the  result  of  which  is  that  when  union  does 
occur  each  party  to  it  contributes  either  an  exactly  equal 
or  an  approximately  equal  amount  of  hereditary  mate- 


GermCelU 


^^■^mi: 


Fig.  9. — Section  across  the  posterior  part  of  an  embryo  dog-fish  (acanthias)  of  3.5  mm.,  to 
show  the  compact  cluster  of  germ  cells  on  one  side.  The  germ  cells  in  later  stages  migrate 
from  this  primative  position,  moving  singly  or  in  small  groups.  Ed,  ectoderm :  Md,  medullary 
canal  or  primitive  spinal  cord;  Nch,  notochord;  A/es,  mesoderm:  £?n<,  entoderm:  X,  cellular 
strand  connecting  the  germ  cell  cluster  with  the  yolk.  (From  Minot  after  Woods,  with  the 
permission  of  the  publishers,  G.  P.  Putnam's  Sons). 

rial.  After  union  has  taken  place  the  fertilized  o\nim 
or  zygote  presently  begins  to  divide,  first  into  two  cells, 
these  again  to  four  and  so  on,  until  by  a  continuation  of 
tliis  process  of  division  with  concomitant  differentiation 
the  whole  body  is  formed.  As  the  animal  develops  by 
repeated  cell  di\dsion  and  differentiation,  it  is  frequently 
found  that  at  the  very  early  stage  the  cells  which  are  to 
be  the  germ  cells  of  the  next  generation  are  clearly  re- 


THE  PROBLEM  39 

cognizable  by  their  structure,  and  often  are  set  aside 
in  a  definite  location  in  the  developing  embrj^o.  Thus, 
to  take  but  a  single  example  of  a  phenomenon  of  wide 
generality,  at  a  very  early  stage  in  the  development  of 
the  dog-fish,  when  the  only  bodily  organs  of  which  even 
the  rudiments  are  recognizable  are  the  beginnings  of  what 
will  presently  become  the  spinal  cord  and  the  back-bone, 


Fig.  10. — First  division  in  egg  of  Cyclops,  showing  at  one  pole  of  spindle  the  granules 
which  mark  the  germ  path.     (From  Child,  after   Amma,   by  permission  of   University  of 

Chicago  Press). 

it  was  showai  by  Woods,  many  years  ago,  that  the  germ 
cells  are  definitely  localized  and  recognizable,  as  shown 
in  Figure  9. 

In  some  forms,  notably  the  round- worm  Ascaris,  va- 
rious Crustacea  and  insects,  the  cells  wliich  are  to  become 
germ  cells  are  visibly  set  apart  from  the  very  first  or  one 
of  the  first  three  or  four  cleavages  of  the  fertilized  ovum. 
For  example,  in  the  case  of  the  crustacean  Cyclops,  Amma 
has  shown  that  the  granules  visible  at  one  pole  in  the 
very  first  division  mark  the  prospective  germ  path,  as 
shown  in  Figure  10. 

In  the  giiat  CJiironormis  the  same  thing  is  visible  at  a 
very  early  cleavage,  according  to  the  observations  of 
Harper.    For  a  comprehensive  and  critical  review  of  the 


40  BIOLOGY  OF  DEATH 

extensive  literature  on  the  Keimhahn  one  should  consult 
the  recent  contributions  of  Hegner  on  the  subject. 

To  condense  a  long  and  complicated  matter  we  may 
state  the  situation  regarding  reproduction  and  death  in 
the  Metazoa  in  this  way.    A  higher,  multicellular  indi\T.- 
dual  may  be  conceived,  from  the  viewpoint  of  the  present 
discussion,  as  composed  of  two  essentially  independent 
portions :  the  germ  cells  on  the  one  hand,  which  are  im- 
mortal in  the  same  sense  that  the  Protozoa  are  immortal, 
and  the  rest  of  the  body,  which  it  is  convenient  to  call 
technically  the  soma,  on  the  other  hand.    The  soma  under- 
goes natural  death  after  an  interval  of  time  which,  as  we 
have  seen,  varies  from  species  to  species.    The  germ  cells 
which  the  individual  bears  in  its  body  at  the  time  of  its 
death  of  course  die  also.    But  this  is  purely  accidental 
death  so  far  as  concerns  the  germ  cells.    Such  of  them  as 
were,  prior  to  the  death  of  the  soma,  enabled  to  unite 
with  other  germ  cells  went  on  living  just  as  does  the 
dividing  Paramecium,    Eeduced  to  a  formula  we  may  say 
that  the  fertilized  o\mm  (united  germ  cells)  produces  a 
soma,  and  more  germ  cells.     The  soma  eventually  dies. 
Some  of  the  germ  cells,  prior  to  that  event,  produce 
somata  and  germ  cells,  and  so  on  in  a  continuous  cycle 
which  has  never  yet  ended  since  the  appearance  of  multi- 
cellular organisms  on  the  earth. 

The  contrast  between  the  protozoan  and  the  metazoan 
method  of  descent  is  shown  in  Figure  11,  which  is  a  modi- 
fication of  a  similar  diagram  originally  due  to  my  col- 
league. Dr.  H.  S.  Jennings. 

The  diagram  represents  the  descent  of  generations. 
The  upper  portion  of  the  diagram  shows  the  mode  of 
descent  in  forms  reproducing  from  organisms  reproduc- 
ing from  a  single  parent.    The  lower,  or  B  portion  of  the 


THE  PROBLEM 


41 


diagram  shows  the  mode  of  descent  in  form  reproducing 
from  two  parents.  The  lines  represent  the  lives  of  indi- 
viduals (as  in  A  diagram),  or  of  germ  cells  (in  the  B 


A 


B 


Fio.  11.  Diagram  to  show  mode  of  descent  in  (A)  unicellular  animals  reproducing  agamic- 
ally,  and  in  (B)  multicellular  animals  reproducing  by  germ  cells.    For  further  explanation  see 

text.  (Modified  from  Jennings). 

diagram)  beginning  at  the  left  and  passing  to  the  right. 
In  the  A  diagram,  which  represents  uniparental  reproduc- 
tion by  fission,  the  line  of  ancestry  traced  back  from  any 
individual  at  the  right  is  always  single,  and  there  is  no 
corpse  to  be  found  anywhere,  each  present  body  trans- 
forming directly  into  the  two  bodies  of  the  next  generation. 


42  BIOLOGY  OF  DEATH 

In  the  B  diagram,  where  we  have  bi-parental  reproduc- 
tion by  the  union  of  germ  cells,  as  in  man,  the  solid  black 
triangles  represent  the  bodies,  or  somata,  and  the  lines 
the  germ  cells.  A  line  of  ancestry  traced  back  from  any 
individual  towards  the  right  end  of  the  diagram  forks 
at  each  generation,  and  in  comparatively  few  generations 
one  has  a  multitude  of  ancestors.  The  bodies  of  one 
generation  have  no  continuity  with  the  bodies  of  the  pre- 
vious or  the  following  generation.  In  each  generation  the 
soma  dies,  while  new  somata  are  reproduced  by  the  union 
of  germ  cells  from  diverse  lines. 

E.  Life  itself  is  a  continuum.  A  break  or  discontin- 
uity in  its  progression  has  never  occurred  since  its  first 
appearance.  Discontinuity  of  existence  appertains  not 
to  life,  but  only  to  one  part  of  the  makeup  of  a  portion 
of  one  large  class  of  living  things.  Tliis  is  certain,  from 
the  facts  already  presented.  Natural  death  is  a  new  thing 
which  has  appeared  in  the  course  of  evolution,  and  its 
appearance  is  concomitant  mth,  and  evidently  in  a  broad 
sense,  caused  by  that  relatively  early  evolutionary  spe- 
cialization which  set  apart  and  differentiated  certain 
cells  of  the  organism  for  the  exclusive  business  of  car- 
rying on  all  functions  of  the  body  other  than  reproduc- 
tion. We  are  able  to  free  ourselves,  once  and  for  all,  of 
the  notion  that  death  is  a  necessarv  attribute  or  inevitable 
consequence  of  life.  It  is  nothing  of  the  sort.  Life  can 
and  does  all  the  time  go  on  without  death.  The  somatic 
death  of  higher  multicellular  organisms  is  simply  the 
price  they  pay  for  the  privilege  of  enjoying  those  higher 
specializations  of  structure  and  function  wliicli  have  been 
added  on  as  a  side  line  to  the  main  business  of  li\ing 
things,  which  is  to  pass  on  in  unbroken  continuity  the 
never-dimmed  fire  of  life  itself. 


THE  PROBLEM  43 

THEORIES   OF   DEATH 

On  the  basis  of  these  five  general  classes  of  facts 
which  have  been  briefly  reviewed  a  whole  series  of  specu- 
lations as  to  the  meaning  of  death  have  been  reared.  The 
first  attempt  at  a  biological  evaluation*  of  the  meaning 
of  death  which  attracted  the  serious  attention  of  scientific 
men  was  that  of  Weismann.  In  his  famous  address  of  1881 
on  the  duration  of  life,  Weismann  propounded  the  thesis 
that  death  was  an  adaptation,  advantageous  to  the  race, 
and  had  arisen  and  was  preserved  by  natural  selection. 
Probably  no  more  perverse  extension  of  the  theory  of 
natural  selection  than  tliis  was  ever  made.  It  appeared, 
however,  just  at  the  time  when  the  post-Darwinian  at- 
tempt to  settle  the  problems  of  evolution  by  sheer  dia- 
lectic was  at  the  zenith  of  its  popularity.  Nowadays  such 
a  doctrine  as  Weismann 's  w^ould  not  receive  so  respectful 
a  hearing. 

Metchnikoff,  whose  views  excited  so  much  popular 
interest  some  years  ago,  held  that  death  was  the  result 
of  intoxication,  arising  from  the  absorption  of  putrefac- 
tive products  of  the  activity  of  intestinal  bacteria.  The 
chief  difficulty  with  this  view  is  that  it  is  demonstrably 
not  true;  either  particularly  in  the  case  of  man,  where 
it  can  easily  be  shown  that  many  statistically  important 
causes  of  death  cannot  possibly  be  accounted  for  under 
it,  or  generally  in  the  animal  kingdom;  because  a  num- 
ber of  cases  are  now  kno^vn  where  a  metazoan  form  can 
be  successfully  made  to  lead  a  completely  aseptic  life, 
and  still  death  occurs  at  about  the  usual  time.  (Of.  Chap- 
ter VIII).    More  speculative  developments  of  the  same 

*  All  excellent  discussion  of  various  theories  of  death,  which  the 
writer,  though  differinjjr  from  some  of  the  conclusions,  has  found  useful 
in  the  preparation  of  this  section,  has  lately  been  given  by  Child  in  his 
"Senescence  and  Rejuvenescence." 


44  BIOLOGY  OF  DEATH 

basic  idea  have  been  presented  by  Jickeli  and  Montgom- 
ery. Both  held  that  because  of  the  mechanical  incomplete- 
ness of  the  processes  of  metabolism,  injurious  and  toxic 
substances  tend  to  accumulate  in  the  cells  of  the  body, 
and  that  senescence  and  death  are  the  results  of 
such  accumulations. 

A  much  broader,  and  in  the  light  of  all  facts  sounder 
view,  is  that  the  determination  of  degrees  of  longevity 
and  of  the  fact  of  death  itself,  is  inherent  in  the  innate, 
hereditarily  determined  biological  constitution  of  the  in- 
dividual and  the  species.  This  view  was  expressed  by 
Johannes  Miiller  a  quarter  of  a  century  ago  in  his  Physi- 
ologies by  Cohnheim  forty  years  later,  and  has  had  many 
later  adherents.  I  shall  return  to  a  discussion  of  it  later. 

There  have  been  a  number  of  theories  of  senescence 
and  death,  differing  widely  in  details,  but  having  the  one 
point  in  common  of  attributing  these  phenomena  to 
orderly  changes  with  advancing  age  in  the  relative  pro- 
portion of  nucleus  to  protoplasm  in  the  cells  of  the  body. 
Here  may  be  mentioned,  without  pausing  to  go  into  de- 
tailed consideration  of  their  different  views,  Verworn, 
Muhlmann,  Richard  Hertwig,  and  Minot. 

Another  group  of  hypotheses,  all  advanced  in  com- 
paratively recent  times  and  associated  with  the  names  of 
Kassomtz,  Conklin,  and  Child,  are  developed  about  the 
metabolic  aspects  of  age  changes.  There  is  observed  a 
decrease  in  assimilatory  capacities  of  cells  with  differen- 
tiation and  age.  These  metabolic  changes  are  regarded 
as  fundamentally  casual  of  the  phenomena  of  senescence 
and  death.  In  this  general  group  of  hypotheses  would 
belong  the  views  of  my  colleague.  Dr.  W.  T.  Howard. 

Benedict  in  a  detailed  investigation  of  senility  in 
plants  reaches  the  conclusion: 


THE  PROBLEM  45 

"that  the  duration  of  life  is  directly  linked  with  the  degree  of  permeability 
in  that  part  of  the  living  cell  which  places  it  in  contact  with  the  universe 
about  it,  and  that  as  the  activities  of  life  proceed  the  cell  is  being  gradually 
entombed  by  an  inevitable  decrease  in  the  permeability  of  its  protoplasm. 
While  decreasing  permeability  furnishes  a  possible  explanation  of  the 
more  obvious  symptoms  of  senilitj^,  it  cannot  be  the  only  degeneration  of 
first  rank.  All  protoplasmic  functions  must  be  involved.  Underlying  these 
primary  causes  of  senile  degeneration  there  must  be  some  general  funda- 
mental cause  from  which  they  spring.  This  fundamental  cause  may  well 
be  the  colloidal  nature  of  protoplasm." 

Delage  and  Jennings  have  considered  that  death  is 
the  result  of  differentiation.  Jennings  has  put  the  matter 
in  this  way 

"the  continuity  of  life  in  the  infusoria  is  in  principle  much  like  that  in 
ourselves,  though  with  differences  in  details.  As  individuals,  the  infusoria 
do  not  die,  save  by  accident.  Those  that  we  now  see  under  our  microscopes 
have  been  living  ever  since  the  beginnings  of  life;  they  come  from  division 
of  previously  existing  individuals.  But  in  just  the  same  sense,  it  is  true 
for  ourselves  that  everyone  that  is  alive  now  has  been  alive  since  the 
beginning  of  life.  This  truth  applies  at  least  to  our  bodies  that  are  alive 
now;  every  cell  of  our  bodies  is  a  piece  of  one  or  more  cells  that  existed 
earlier,  and  thus  our  entire  body  can  be  traced  in  an  unbroken  chain  as 
far  back  into  time  as  life  goes.  The  difference  is  that  in  man  and  other 
higher  organisms  there  have  been  left  all  along  the  way  great  masses  of 
cells  that  did  not  continue  to  live.  These  masses  that  wore  out  and  died 
,are  what  we  call  the  bodies  of  the  persons  of  earlier  generations;  but 
our  own  bodies  are  not  descended  by  cell  division  from  these;  they  are  the 
continuation  of  cells  that  have  kept  on  living  and  multiplying  from  the 
earliest  times,  just  as  have  the  existing  infusoria." 

Jennings'  views  regarding  senescence  in  the  protozoa 
will  be  discussed  in  the  next  chapter. 

Unicellular  organisms,  as  we  have  seen,  do  not  nor- 
mally experience  natural  death.  In  the  higher  organisms 
there  has  been  a  progressive  setting  apart  of  cells  and 
tissues  to  perform  particular  vital  functions  with  a  con- 
sequent loss  of  the  ability  to  perform  all  \dtal  functions 
independently .  As  soon  as  any  one  of  these  cells  or  tissues 
begins,  for  any  accidental  cause  whatever,  to  fail  to  per- 


46  BIOLOGY  OF  DEATH 

form  its  special  function  properly,  it  upsets  the  delicate 
balance  of  the  whole  associated  community  of  cells  and  tis- 
sues. Because  of  the  differentiation  and  specialization  of 
function,  the  parts  are  mutually  dependent  upon  each 
other  to  keep  themselves  and  the  whole  going.  Conse- 
quently any  disturbance  in  the  balance  wliich  is  not 
promptly  righted  by  some  regulatory  process  must  even- 
tually end  in  death. 

Since  the  publication  of  this  material  in  serial  form 
an  objection  to  the  foregoing  statement  has  been  sug- 
gested on  the  ground  that  differentiation  per  se  does  not 
appear  to  the  critic  to  have  much  to  do  with  the  question  of 
natural  death  in  the  Metazoa.  To  quote ;  ^  ^  rather  it  is  the 
failure  after  differentiation  to  keep  up  indefinitely  the 
state  reached.  If,  from  any  internal  or  external  accident, 
the  differentiated  part  suffers  injury,  the  injury  cannot 
be  made  good  any  more,  since  in  certain  organs  this  power 
has  been  lost.  Hence,  in  time,  loss  after  loss  occurs  and 
the  machine  wears  out.  The  protozoan  is  as  highly  differ- 
entiated as  any  cell  of  a  metazoan  (or  much  more  so) ;  but 
since  it  ^'multiplies  by  di\TLding,"  it  has  retained  the 
power  to  make  good  any  loss.  Therefore,  it  is  not  the 
differentiation  per  se,  but  the  loss  of  power  to  repair 
that  produces  senescence." 

This  seems  to  me  to  be  in  the  main  only  a  somewhat 
different  form  of  statement  of  precisely  the  idea  that  I 
have  endeavored  to  express.  When  I  have  used  the  term 
*' differentiation"  in  this  connection,  I  have  always  had 
in  mind,  as  one  of  its  most  important  physiological  con- 
comitants, just  the  thing  spoken  of  above.  Furthermore, 
whether  the  protozoan  cell  is  as  liighly  differentiated  as 
a  metazoan  cell,  is  not  to  the  point  at  all.  For,  to  have 
any  pertinence  so  far  as  the  present  issue  is  concerned, 
the  comparison  must  be  between  the  differentiated  proto- 


THE  PROBLExM  47 

zoan  cell,  and  the  whole  metazoau  soma,  not  one  of  its 
constituent  cells.  In  the  protozoan,  all  the  dilferentia- 
tions  are  in  and  a  part  of  one  single  cell  operating  as  one 
metabolic  unit,  of  small  absolute  size,  and  consequently 
easier  and  more  labile  internal  physico-chemical  regula- 
tion. In  the  metazoan  soma  we  have  organ  differentia- 
tion, with  the  constituent  cells  in  each  organ  highly 
specialized  functionally,  and  dependent  upon  the  nor- 
mal functional  activity  of  wholly  other  organs  in  order 
that  they  may  keep  going  at  all.  Remove  these 
tissue  cells  from  the  soma,  and  provide  them  with  an 
abundance  of  suitable  nourislmaent  and  oxygen,  as  in 
tissue  cultures,  and,  so  far  as  the  evidence  now  available 
indicates,  they  will  live  forever  (cf.  Chapter  II). 

Consider  for  a  moment  the  most  higlily  differentiated 
protozoan  known,  on  the  one  hand,  and  man,  on  the  other 
hand,  purely  as  physico-chemical  machines,  wliich  only 
keep  going  if  the  internal  balances  and  adjustments  are, 
in  each  case,  held  within  a  narrow  zone  of  normality. 
Quite  aside  from  any  question  of  their  different  modes 
of  reproduction,  the  two  machines  are  not  equivalent, 
as  machines,  because  of  :(a)  unicellular  versus  multicel- 
lular structure,  (b)  great  absolute  difference  in  size  of 
the  whole  machines,  with  consequent  requirement  of  an 
enormously  more  complex  internal  regulatory  mechanism 
in  the  one  case  than  in  the  other,  whatever  the  inherent 
nature  of  this  mechanism  may  be. 

Essentially  the  same  view  of  the  matter  as  tliat 
held  by  the  present  writer  has  been  well  set  f  ortli  by  Loeb 
in  liis  most  recent  paper  on  the  subject.    He  says : 

"All  this  points  to  the  idea  that  death  is  not  inherent  in  the  individual 
cell,  but  is  only  the  fate  of  more  complicated  organisms  in  which  different 
types  of  cells  or  tissues  are  dependent  upon  each  other.  In  this  case  it 
seems  to  happen  that  one  or  certain  types  of  cells  produce  a  substance  or 
substances  which  gradually  become  harmful  to  a  vital  organ  like  the  res- 


48  BIOLOGY  OF  DEATH 

piratory  center  of  the  medulla,  or  that  certain  tissues  consume  or  destroy 
substances  which  are  needed  for  the  life  of  some  vital  organ.  The  mischief 
of  death  of  complex  organisms  may  then  be  traced  to  the  activity  of  a 
black  sheep  in  the  society  of  tissues  and  organs  which  constitute  a  com- 
plicated multicellular  organism." 

At  this  point  I  shall  not  stay  to  discuss  critically  each 
of  the  hypotheses  so  summarily  reviewed.  Instead,  I 
shall  make  bold  to  state  somewhat  categorically  my  own 
views  on  the  origin  and  meaning  of  death  and  the  deter- 
mination of  longevity ;  and  in  what  follows,  shall  endeavor 
to  set  forth  in  orderly  array  the  evidence  which  seems  to 
me  to  support  these  views.  In  this  process,  the  relations 
of  what  I  shall  suggest  to  the  conclusions  of  earlier  inves- 
tigators mil,  I  tliink,  sufficiently  appear. 

Let  us  consider,  then,  the  following  picture  of  life 
and  death: 

1.  Life  itself  is  inherently  continuous. 

2.  Living  things,  whether  single-celled  or  many- 
celled  organisms,  are  essentially  only  physico-chemical 
machines  of  extraordinary  complexity ;  but  regardless  of 
their  degree  of  complexity  only  amenable  to,  and 
activated  in  accordance  with,  physical  and  chemical  laws 
and  principles. 

3.  The  discontinuity  of  death  is  not  a  necessary  or 
inherent  adjunct  or  consequence  of  life,  but  is  a  rela- 
tively new  phenomenon,  which  appeared  only  when  and 
because  differentiation  of  structure  and  function  appeared 
in  the  course  of  evolution. 

4.  Death  necessarily  occurs  only  in  such  somata  of 
multicellular  organisms  as  have  lost,  through  differentia- 
tion and  specialization  of  function,  the  power  of  repro- 
ducing each  part  if  it,  for  any  accidental  reason  breaks 
down  or  is  injured;  or  still  possessing  such  power  in  their 
cells,  have  lost  the  necessary  mechanism  for  separating  a 


THE  PROBLEM  49 

part  of  the  soma  from  the  rest  for  purposes  of  agamic 
reproduction. 

5.  Somatic  death  results  from  an  organic  disharmony 
of  the  whole  organism,  initiated  by  the  failure  of  some 
organ  or  part  to  continue  in  its  normal  harmonious  func- 
tioning in  the  entire  differentiated  and  mutually  depend- 
ent system.  This  functional  breakdown  of  a  part  may 
be  caused  in  a  multitude  of  ways  from  external  or  internal 
sources.  It  may  manifest  itself  in  a  great  variety  of 
ways  both  structurally  and  functionally.  Many  of  these 
manifestations  which  have  been  regarded  as  causes  of 
senescence,  may  more  truly  be  considered  concomitant 
attributes  of  senescence. 

6.  As  a  consequence  of  our  second  thesis  which  postu- 
lated life  to  be  a  mechanism,  death,  whether  of  a  single 
somatic  cell  or  of  a  whole  soma,  is  a  result  of  physico- 
chemical  changes  in  the  cell  or  organism;  and  these 
changes  are  in  accordance  with  ordinary  physico- 
chemical  laws  and  principles. 

7.  The  time  at  which  natural  death  of  the  soma  occurs 
is  determined  by  the  combined  action  of  heredity  and 
environment.  For  each  organism  there  is  a  specific  long- 
evity determined  by  its  inherited  physico-chemical  con- 
stitution. This  specific  longe\dty  is  capable  of  modifica- 
tion, witliin  relatively  narrow  limits,  as  a  result  of  the 
impact  of  environmental  forces ;  the  chief  mode  of  action 
of  the  environment  being  in  the  direction  of  determining 
the  rate  at  which  the  inherited  endo\\Tnent  is  used  up. 

For  no  one  of  the  separate  elements  of  this  picture  can 
I  claim  any  particular  originality.  Most  of  them  would 
probably  be  agreed  to  at  once,  at  least  by  some  biologists. 
The  need  is  for  a  synthesizing  into  a  consistent  whole  of 
a  wide  range  of  data,  which  have  accumulated  in  various 
4 


50  BIOLOGY  OF  DEATH 

fields  of  biology,  about  death  and  the  duration  of  life. 
Such  a  synthesis  will  be  attempted  in  what  follows. 
Generally,  those  who  have  speculated  about  the  biology 
of  death  have  drawn  their  evidence  from,  or  at  least  had 
their  thinking  largely  colored  by  the  facts  in  a  relatively 
small  part  of  the  whole  field.  In  particular,  few  biologists 
have  any  detailed  knowledge!  of  the  most  impressive 
mass  of  material,  both  in  respect  of  quality  and  quantity, 
which  exists  regarding  the  duration  of  life  of  any  organ- 
ism. I  refer,  of  course,  to  the  enormous  volume  of 
rather  exact  data  regarding  human  mortality.  Much  of 
this  material,  to  be  sure,  wants  proper  analysis,  not 
only  mathematical  but  biological.  But,  that  it  is  a  rich 
material  admits  of  no  doubt. 


CHAPTER  II 

CONDITIONS  OF  CELLULAR  IMMORTALITY 

In  the  preceding  chapter  it  was  pointed  out  that  the 
germ  cells  of  higher  organisms  are  potentially,  and  under 
certain  conditions  in  fact,  immortal.  What  are  the  con- 
ditions of  immortality  in  this  case?  Are  they  such  as 
to  support  the  thesis  that  the  processes  of  mortality  are 
essentially  physico-chemical  in  nature,  and  follow 
physico-chemical  laws? 

ARTIFICIAL   PARTHENOGENESIS 

The  most  essential  condition  of  tliis  immortality  of 
germ  cells  w^as  mentioned,  but  not  particularly  empha- 
sized. It  is  that  two  germ  cells,  an  ovum  and  a  spermato- 
zoon unite,  the  process  of  union  being  called  fertilization. 
Ha^^ing  united,  if  they  then  find  themselves  in  appro- 
priate environmental  conditions,  development  goes  on; 
new  germ  cells  and  a  soma  are  formed,  and  the  same 
process  keeps  up  generation  after  generation.  Now,  while 
union  of  the  germ  cells  is  generally  and  in  most  organisms 
an  essential  condition  of  this  process,  it  is  also  true  that 
in  a  few  forms  of  animal  life,  mostly  found  among  the 
invertebrates,  development  of  the  o\Tim  can  take  place 
without  any  preceding  fertilization  by  a  spermatozoon. 
The  process  of  reproduction,  in  this  case  is  called  par- 
the  no  genesis.   In  a  number  of  forms  in  which  partheno- 
genesis never  occurs  normally,  so  far  as  is  known,  it  can 
be  induced  by  appropriate  extraneous  procedures.    The 
discovery  of  this  extraordinarily  interesting  and  impor- 
tant fact  for  a  number  of  organisms,  and  the  careful 

61 


52  BIOLOGY  OF  DEATH 

working  out  of  its  physico-chemical  basis,  we  owe  to  Dr. 
Jacques  Loeb,  of  the  Eockefeller  Institute  for  Medical 
Eesearch.  Artificial  parthenogenesis  may  be  induced, 
as  Guyer,  Bataillon  and  Loeb  have  shown,  even  in  so 
highly  organized  a  creature  as  the  frog,  and  the  animal 
may  grow  to  full  size.  The  frogs  shown  in  Figure  12,  while 
they  present  an  appearance  much  the  same  as  that  of 
any  other  frog  of  the  same  species,  differ  in  the  rather 
fundamentally  important  respect  that  they  had  no  father. 
The  role  of  a  father  was  played  in  these  cases  by  an 
ordinary  dissecting  needle.  Unfertilized  eggs  from  a 
virgin  female  were  gently  pricked  with  a  sharply  pointed 
needle.  This  initiation  of  the  process  of  development  took 
place  March  16,  1916,  in  one  case,  and  February  27,  1917, 
in  the  other.  The  date  of  death  was,  in  the  first  case.  May 
22, 1917,  and  in  the  other  March  24,  1918. 

In  the  course  of  Loeb's  studies  of  parthenogenesis  in 
lower  marine  invertebrates,  he  became  interested  in  the 
question  of  the  death  of  the  germ  cells  which  had  failed 
to  unite,  or,  having  united,  failed  of  appropriate  envi- 
ronmental conditions.  His  researches  throw  light  on  some 
of  the  conditions  of  cellular  death,  and  on  that  account 
they  may  be  reviewed  briefly  here.  He  found  that  the 
unfertilized  mature  eggs  of  the  sea-urchin  die  compara- 
tively soon  when  deposited  in  sea- water.  The  same  eggs, 
however,  live  much  longer,  and  will,  if  appropriate  sur- 
rounding conditions  are  provided,  go  on  and  develop  an 
adult  organism,  if  they  are  caused  to  develop  artificially 
by  chemical  means  or  naturally  by  fertilization.  Loeb 
concluded  from  this  that  there  are  two  processes  going 
on  in  the  egg.  He  maintained,  on  the  one  hand,  that  there 
are  specific  processes  leading  to  death  and  disintegration; 
and,  on  the  other  hand,  processes  which  lead  to  cell  di\d- 


I 

I 


o 
to 


OR 


CONDITIONS  OF  CELLULAR  IMMORTALITY  53 

sion  and  further  development.  The  latter  processes  may 
be  regarded  as  inhibiting  or  modifying  the  mortal  pro- 
cess. Loeb  and  Lems*  undertook  experiments,  based 
upon  this  view,  to  see  whether  it  would  be  possible  by 
chemical  treatment  of  the  egg  to  prolong  its  life.  Since 
in  general  specific  Life  phenomena  are  perhaps,  on  the 
chemical  side,  chiefly  catalytic  phenomena,  it  was  held 
to  be  reasonable  that  if  some  substance  could  be  brought 
to  act  on  the  egg^  which  would  inhibit  such  phenomena 
without  permanently  altering  the  constitution  of  the 
living  material,  the  life  of  the  cell  should  be  considerably 
prolonged.  The  first  agent  chosen  for  trial  was  potassium 
cyanide,  KCN.  It  was  known  that  this  substance  weakened 
or  inhibited  entirely  a  number  of  enzymatic  processes  in 
living  material,  without  materially  or  permanently  alter- 
ing its  structure. 

It  was  found  that,  normally,  the  unfertilized  egg  of  the 
sea-urchin  would  live  in  sea-water  at  room  temperature, 
and  maintain  itself  in  condition  for  successful  fertiliza- 
tion and  development,  up  to  a  period  of  about  twenty-three 
hours.  After  that  time  the  eggs  began  to  weaken.  Either 
they  could  not  be  successfully  fertilized,  or  if  they  were 
fertilized,  development  only  went  on  for  a  short  time. 
After  32  hours,  the  eggs  could  not,  as  a  rule,  be  fertilized 
at  all.  The  experiment  was  then  tried  of  adding  to  the 
sea-water,  in  which  the  unfertilized  eggs  were  kept, 
small  amounts  of  KCN  in  a  graded  series,  and  then  exam- 
ining the  results  of  fertilizations  undertaken  after  a  stay 
of  the  unfertilized  eggs  of  75  hours  in  the  solution.  It 
will  be  noted  that  this  period  of  75  hours  is  more  than 
three  times  the  normal  duration  of  life  of  the  cell  in 
normal  sea-water.  The  results  of  this  experiment  are 
shown  in  summary  form  in  Table  4. 


54 


BIOLOGY  OF  DEATH 

TABLE  4 


Experiments  oj  Loeh  and  Lewis  on  the  Prolongation  of  Life  of  the  Sea-urchin 

Egg  by  KCN 


Concentration  of 

Result  of  fertilization  after  a  75  hours'  stay 

KCN 

in  the  solution 

Pure   sea 

-water 

No  egg  segments 

n/64000 

KCN 

No  egg  segments 

n/16000 

KCN 

No  egg  segments 

n/8000 

KCN 

Very  few  eggs  show  a  beginning  of  seg- 
mentation 

n/4000 

KCN 

Very  few  eggs  show  a  beginning  of  seg- 
mentation 

n/2000 

KCN 

Few  eggs  go  through  the  early  stages  of 
segmentation 

n/lOOO 

KCN 

Many  eggs  segment  and  develop  into  swim- 
mmg  larvae 

n/750 

KCN 

Many  eggs  segment  and  develop  into  swim- 
ming larvae 

n/400 

KCN 

A  few  eggs  develop  into  swimming  larvae 

n/300 

KCN 

No  egg  segments 

n/250 

KCN 

No  egg  segments 

11/200 

KCN 

No  egg  segments 

n/100 

KCN 

No  egg  segments 

From  tliis  table  it  is  seen  that  in  concentrations  of 
KCN  from  n/750  to  n/1000  the  eggs  developed  perfectly 
into  swimming  larvae.  In  other  words,  by  the  addition 
of  this  very  small  amount  of  KCN,  the  life  period  has 
been  prolonged  to  three  times  what  it  would  normally 
be  under  the  same  environmental  conditions.  Concen- 
trations of  KCN  weaker  than  n/1000  were  incapable  of 
producing  this  result,  or  at  best,  if  development  started, 
the  process  came  very  quickly  to  an  end.  In  stronger 
concentrations  than  n/400  the  eggs  were  evidently  poi- 
soned, and  no  development  occurred. 

Other  experiments  of  Loeb's  show  that  the  lethal 
effects  of  various  toxic  agents  upon  the  egg  cell  may  be 
inhibited  or  postponed  for  a  relatively  long  time,  by 


CONDITIONS  OF  CELLULAR  IMMORTALITY  55 

suitable  chemical  treatment,  such  as  lack  of  oxygen,  KCN, 
or  chloral  hydrate.  A  typical  experiment  of  this  kind 
made  upon  the  sea-urchin,  Strongylocentrotus  pur  pur  at  us 
may  be  quoted: 

EfjfTs  were  fertilized  with  sperm  and  put  eleven  minutes  later  into 
three  flasks,  each  of  which  contained  100  c.  o.  of  sea-water  +  16  c.  c.  2-y2 
m  CaClj.  One  flask  was  in  contact  with  air,  while  the  other  two  flasks 
were  connected  with  a  hydrogen  generator.  The  air  was  driven  out  from 
these  two  flasks  before  the  beginning  of  the  experiment.  The  eggs  were 
transferred  from  one  of  these  flasks  after  four  hours  and  fourteen  minutes, 
from  the  second  flask  after  five  hours  and  twenty-nine  minutes,  into  normal 
(aerated)  sea -water.  The  eggs  that  had  been  in  the  hypertonic  sea -water 
exposed  to  air  were  transferred  simultaneously  with  the  others  into 
separate  dishes  with  aerated  normal  sea-water.  The  result  was  most 
striking.  Those  eggs  that  had  been  in  the  hypertonic  sea-water  with  air 
were  all  completely  disintegrated  by  *'  black  cytolysis."  Ten  per  cent, 
of  the  eggs  had  been  transformed  into  ''shadows"  (white  cytolysis).  It 
goes  without  saying  that  all  the  eggs  that  had  been  in  the  aerated  hyper- 
tonic sea-water  five  and  a  half  hours  were  also  dead.  The  eggs  that  had 
been  in  the  same  solution  in  the  absence  of  oxygen  appeared  all  normal 
when  they  were  taken  out  of  the  solution,  and  three  hours  later — the 
temperature  was  only  15°C. — they  were  all,  without  exception  in  a  per- 
fectly normal  two-  or  four-cell  stage.  The  further  development  was  also 
in  most  cases  normal.  They  swam  as  larvae  at  the  surface  of  the  vessel 
and  went  on  the  third  day  (at  the  right  time)  into  a  perfectly  normal 
pluteus  stage,  after  which  their  observation  was  discontinued.  Of  the 
eggs  that  had  been  five  and  a  half  hours  in  the  hypertonic  sea-water 
deprived  of  oxygen,  about  90  per  cent,  segmented. 

Let  US  consider  one  more  illustration  from  Loeb's 
work  in  this  field.  Normally,  in  the  forms  mth  wliich 
he  chiefly  worked,  sea-urchin,  starfish,  and  certain  mol- 
luscs, an  absolutely  essential  condition  for  the  continua- 
tion of  life  of  the  germ-cells  after  they  are  discharged 
from  the  body  is  that  two  cells,  the  o\^im  and  the  sper- 
matozoon, shall  unite  in  noraial  fertilization.  Put  in 
another  way,  parthenogenesis  does  not  normally  occur  in 
these  forms.  Fertilization  is  an  essential  condition  for 
the  continuation  of  life  and  development.     But  Loeb's 


56  BIOLOGY  OF  DEATH 

painstaking  and  brilliant  researches,  extending  over  a 
number  of  years,  show  that  when  we  say  that  fertilization 
is  an  essential  condition  for  the  continued  life  of  the 
germ-cells  outside  the  body,  our  language  tends  to  ob- 
scure the  most  important  fact,  which  is  simply  that  for 
the  continuation  of  life  in  these  cells  only  certain  internal 
physico-chemical  conditions  and  adjustments  must  be 
realized.  It  makes  no  essential  difference  to  the  result 
whether  these  conditions  are  realized  through  the 
intervention  of  the  sperm,  as  in  normal  fertiliza- 
tion, or  by  purely  artificial  chemical  methods  initiated, 
controlled  and  directed  at  every  step  by  human  agency. 
We  can,  in  other  words,  regard  all  cases  of  suc- 
cessful artificial  parthenogenesis  as  fundamentally  a  con- 
tribution to  the  physiology  of  natural  death,  and  a  demon- 
stration of  its  essentially  mechanistic  basis.  The  condi- 
tions of  continued  existence  are  physical  and  chemical, 
and  controllable  as  such.  The  methods  finally  worked  out 
as  optimum  afford  a  complete  demonstration  of  the  thesis 
we  have  just  stated.  Thus,  for  example,  the  unfertilized 
egg  of  the  sea-urchin,  Strongyloce^itrotus  purpuratus, 
will  continue  in  life  and  develop  perfectly  normally  if  it 
is  subjected  to  the  following  treatment:  The  eggs  are 
first  placed  in  sea-water  to  which  a  definite  amount  of 
weak  solution  of  butyric  acid  has  been  added  (50  cc.  of 
sea- water  -f  2.8  cc.  n/10  butyric  acid).  In  this  solution 
at  15°  C.  the  eggs  are  allowed  to  remain  from  1%  to  3  or 
4  minutes.  They  are  then  transferred  to  normal  sea-water, 
in  which  they  remain  from  15  to  20  minutes.  They  are 
then  transferred  for  30  to  60  minutes  at  15°  C.  to  sea-water 
which  has  had  its  osmotic  pressure  raised  by  the  addition 
of  some  salts  (50  cc.  of  sea-wa.ter+8  cc  of  2i/^  m  NaCl,  or 
2%  m  NaCl+KCL-fCaCl2  in  the  proportion  in  which  these 


CONDITIONS  OF  CELLULAR  IMMORTALITY  57 

salts  exist  in  sea-water).  After  the  stay  of  from  30  to  60 
minutes  in  this  sohition,  the  egs;s  are  transferred  hack  to 
normal  sea-water,  the  transferring  being  in  batclies  at 
intervals  of  3  to  5  mimites  between  each  batch  transferred. 
It  is  then  fonnd  that  those  eggs  Avhich  have  been  just  the 
right  length  of  time  in  the  hypertonic  sea- water  develop 
into  perfectly  normal  sea-urchin  larva^.  In  other  words, 
we  have  here  a  detinite  and  known  physico-chemical  pro- 
cess completely  replacing  what  was,  before  this  work, 
universally  regarded  as  a  peculiarly  vital  process  of 
extraordinary  complexity,,  ^probably  beyond  power  of 
human  control. 

These  three  examples  from  Loeb's  work  on  the  sub- 
ject of  prolongation  of  life  in  the  egg  cell  mil  sufiSce  for 
our  present  purposes.  The  lesson  which  they  teach  is 
plain,  and  is  one  which  has,  as  will  be  readily  perceived, 
a  most  important  bearing  upon  the  general  concept  of 
life  and  death  outlined  in  the  preceding  chapter.  The 
experiments  demonstrate  that  the  conditions  essential  to 
continued  life  of  the  germ-cells  outside  the  body  are  phy- 
sico-chemical conditions,  and  that  when  these  cells  die  it 
is  because  the  normal  physico-chemical  machinery  for  the 
continuation  of  life  has  either  broken  doA\Ti,  or  has  not 
been  given  the  proper  activating  chemical  conditions. 

Lack  of  space  alone  prevents  going  in  detail  into  an- 
other extremely  interesting  and  important  development 
of  this  subject,  due  to  Dr.  Frank  R.  Lillie  of  the  Univer- 
sity of  Chicago.  He  has,  in  recent  years  made  a  thorough 
analysis  of  the  biological  factors  operating  when  the  egg 
of  the  sea-urchin  is  normally  fertilized  by  a  spermato- 
zoon. The  conception  of  the  process  of  fertilization  to 
wliich  Lillie  comes  is  ^Hhat  a  substance  borne  by  the  egg 
(fertilizin)  exerts  two  kinds  of  actions:  (1)  an  agglutin- 


58  BIOLOGY  OF  DEATH 

ating  action  on  the  spermatozoon  and  (2)  an  activating 
action  on  the  egg.  In  other  words,  the  spermatozoon  is 
conceived,  bv  means  of  a  substance  which  it  bears  and 
which  enters  into  union  with  the  f ertilizin  of  the  egg,  to 
release  the  activity  of  this  substance  within  the  egg.^^ 
From  the  standpoint  of  the  present  discussion  it  is  ob- 
vious that  Lillie's  results  so  far  present  nothing  which 
in  any  way  disturbs  the  conclusion  we  have  reached  as 
to  the  essentially  physico-chemical  nature  of  the  processes 
which  condition  the  continuation  of  life  and  development 
of  the  egg. 

TISSUE  CULTUKE  IN  VITRO 

Let  us  turn  now  to  another  question.  Are  the  germ- 
cells  the  only  cells  of  the  metazoan  body  which  possess 
the  characteristic  of  potential  immortality!  There  is 
now  an  abundance  of  evidence  that  such  is  not  the  case, 
but  that,  on  the  contrary,  there  are  a  number  of  cells  and 
tissues  of  the  body,  which,  under  appropriate  conditions, 
may  continue  living  indefinitely,  except  for  the  purely 
accidental  intervention  of  lethal  circumstances.  Every 
child  knows  that  all  the  tissues  do  not  die  at  the  same  time. 
It  is  proverbial  that  the  tail  of  the  snake,  whose  head  and 
body  have  been  battered  and  crushed  until  even  the  small 
boy  is  willing  to  admit  that  the  job  of  killing  is  complete, 
*  *  will  not  die  until  the  sun  goes  down. ' '  Galvani  's>  famous 
experiment  mth  the  frog's  legs  only  succeeded  because 
some  parts  survive  after  the  death  of  the  organism  as 
a  whole.  As  Harrison  points  out  **  Almost  the  whole  of 
our  knowledge  of  muscle-nerve  physiology,  and  much  of 
that  of  the  action  of  the  heart,  is  based  upon  experiments 
with  surviving  organs ;  and  in  surgery,  where  we  have  to 
do  with  changes  involved  in  the  repair  of  injured  parts, 


^7"-J'^- — P'PfP  of  tissue  from  frog  emliryo  cultivaf cd  in  Ivmph,  two  <lays  oI«l 
he  dark  portion  shows  oriKinal  hit  of  tissiu;.     LiKiitei  portions  arc  new  Kiowth 

(.From  Harrison.) 


Fig   14  -Group  of  nerve  fibers  which  have  grown.from  an  isolated  piece  of  neural  tube  of  a  chick 
tiG.li.     oroupo  embryo.     (From  Harrison  after  Burrows.) 


CONDITIONS  OF  CELLULAR  IMMORTALITY  59 

including  processes  of  growth  and  differentiation,  the 
power  of  survival  of  tissues  and  organs  and  their  trans- 
plantability  to  strange  regions,  even  to  other  individuals, 
has  long  formed  the  basis  of  practical  procedures." 

The  first  successful  cultures  of  somatic  cells  and  tis- 
sues outside  the  body  were  those  of  Leo  Loeb,  described 
in  1897.  His  first  method  consisted  in  cultivating  the 
tissues  in  appropriate  media  in  test  tubes.  Later  he  used 
also  another  method,  which  involved  the  transplantation 
of  the  solid  medium  and  the  tissue  into  the  body  of  an- 
other animal.  What  has  been  regarded  as  a  defect  of 
both  these  methods  is  that  they  do  not  permit  the  contin- 
ued observation  of  the  cells  of  the  growing  cultured  tissue. 
To  Harrison  is  due  the  development  of  a  method  which 
does  permit  such  study.  In  1907  he  announced  the  dis- 
covery that  if  pieces  of  the  developing  nervous  system  of 
a  frog  embryo  were  removed  from  the  body  with  fine 
needles,  under  strictly  aseptic  precautions,  placed  on  a 
sterile  cover  slip  in  a  drop  of  frog  lymph,  and  the  cover 
slip  then  inverted  over  a  hollow  glass  slide,  that  the  tis- 
sues would  remain  alive  for  many  days,  grow  and  exhibit 
remarkable  transformations.  By  tliis  technique  it  was 
possible  to  study  the  changes  with  a  liigh  power  micro- 
scope and  photograph  them. 

Figure  13  is  a  general  view  of  one  of  these  tissue  cul- 
tures two  days  old.  It  shows  a  piece  of  nervous  tissue 
from  the  frog  embryo,  with  cells  gro\nng  out  from  it 
into  the  lymph.  The  lighter  portions  are  the  new  cells. 
In  his  remarkable  monograph  Harrison  shows  nerve 
cells  developing  fibers  at  first  thickened,  but  presently 
becoming  of  normal  character  and  size.  At  the  ends  are 
pseudopodial  processes,  by  which  the  growing-  fiber  at- 
taches itself  to  the  cover  slip  or  other  solid  bodies.    Fig- 


60  BIOLOGY  OF  DEATH 

ure  14  shows  a  particularly  beautiful  nerve  fiber  prepar- 
ation made  by  Burrows. 

The  fibers  grew  from  a  preparation  of  the  embryonic 
nervous  system  of  the  chick.  There  can  be  no  doubt,  as 
these  figures  so  clearly  show,  of  the  life  of  these  cells 
outside  the  body,  or  of  the  normality  of  their  develop- 
mental and  growth  processes. 

Under  the  guidance  of  Harrison,  'another  worker, 
Burrows,  improved  the  technique  of  the  cultivation  of 
tissues  outside  the  body,  first  by  using  plasma  from  the 
blood  instead  of  lymph  and  later  in  various  other  ways. 
He  devised  an  apparatus  for  affording  the  tissue  culture 
a  continuous  supply  of  fresh  nutrient  medium.  There  is 
in  this  apparatus  a  large  culture  chamber  which  takes 
the  place  of  the  plain  hanging  drop  in  an  "hermetically 
sealed  cell.  On  the  top  of  this  culture  chamber  there  is 
a  wick,  which  carries  the  culture  fluid  from  a  supplying 
chamber  and  discharges  it  into  a  receiving  chamber.  The 
tissue  is  planted  among  the  fibers  of  the  wick,  which  are 
pulled  apart  where  it  crosses  the  top  of  the  chamber. 
The  whole  system  is  kept  sterile  and  so  arranged  that 
the  growing  tissue  can  be  kept  under  observation  with 
high  powers  of  the  microscope.  The  nutrient  medium 
may  be  modified  at  will,  and  the  effects  of  known  sub- 
stances upon  the  cellular  activities  of  every  sort  may 
be  studied. 

Burrows  began  his  investigations  in  this  field  on  the 
tissues  of  the  embryo  chick.  With  the  success  of  these 
cultures  was  established  the  fact  that  the  tissues  of  a 
warm  blooded  animal  were  as  capable  of  life,  develop- 
ment, and  growth  outside  the  body  as  were  those  of  cold- 
blooded animals,  such  as  the  frog.  Burrows  succeeded 
in  cultivating  outside  the  body,  cells  of  the  central  nervous 


■■"■ift-r  ■■ 


% 


Fio.  15. — Human  fonn<  ctivo  tissue  rolls  fixed  and  stained  with  Gicnisa  stain.  The  culture  was 
made  by  e.xtirpatiufr  tlic  (■crilral  jxirtion  of  culture  2sr)  in  its  Kith  i)assavre.  washing  the  renuiininn 
portionOf  tiie  cullui-e  with  ijin^icr  solution  wit IiduI  removing  if  from  the  eover-ulass.  and  dro|>- 
ping  on  tresh  plasm  ami  extract.  The  preparation  shows  the  extent  of  growth  ol)»ain«'d  in  Is  hours 
from  peripheral    cells  remaining  after    extirjiation    of    t  he  fraLMiient .     (.\fter  l.oscc  and  I^lielinu.) 


I 


CONDITIONS  OF  CELLULAR  LMMORTALITY  01 

system,  the  heart,  and  mesenchymatoiis  tissue  of  the 
chick  embryo.  At  the  same  time  Carrel  was  carrying 
on  studies  in  this  same  direction  at  the  Rockefeller  In- 
stitute. In  his  laboratory  were  made  the  first  successful 
cultures  in  vitro  of  the  adult  tissues  of  mammals.  He 
developed  a  method  of  culture  on  a  plate  which  permitted 
the  growing  of  large  quantities  of  material.  He  found 
that  almost  all  the  adult  and  embryonic  tissues  of  dog, 
cat,  chicken,  rat,  guinea  pig,  and  man  could  be  cultivated 
in  vitro.  Fig-ure  15  shows  a  culture  of  human  tissue, 
made  at  the  Rockefeller  Institute.  I  am  indebted  to 
Doctor  Carrel  and  Doctor  Ebeling  for  permission  to  pre- 
sent this  photograph  here. 

According  to  the  nature  of  the  tissues  cultivated,  con- 
nective or  epithelial  cells  were  generated,  which  grew  out 
into  the  plasma  medium  in  continuous  layers  or  radiating 
chains.  Not  only  could  normal  tissues  be  cultivated  but 
also  the  cells  of  pathological  growths  (cancer  cells). 
It  has  been  repeatedly  demonstrated  that  normal  cell 
division  takes  place  in  these  tissues  cultivated  outside  the 
body.  The  complex  process  of  cell  division,  which  is 
technically  called  mitosis,  has  been  rightly  regarded  as 
one  of  the  most  characteristic,  because  complicated  and 
unique,  phenomena  of  normal  life  processes.  Yet  this 
process  occurs  with  perfect  normality  in  cells  cultivated 
outside  the  body.  Tissues  from  various  organs  of  the 
body  have  been  successfully  cultivated,,  including  the 
kidney,  the  spleen,  the  thyroid  gland,  etc.  Burrows  was 
even  able  to  demonstrate  that  the  isolated  heart  muscle 
cells  of  the  chick  embrvo  can  divide  as  well  as  differen- 
tiate,  and  beat  rhythmic  ally  in  the  culture  medium. 

Perhaps  even  more  remarkable  than  the  occurrence 
of  such  physiological  activity  as  that  of  the  heart  muscle 


62  BIOLOGY  OF  DEATH 

cells  in  vitro  is  the  fact  that  in  certain  lower  forms  of  life 
a  small  bit  of  tissue  or  even  a  single  cell,  may  develop  in 
culture  into  a  whole  organism,  demonstrating  that  the 
capacity  of  morphogenesis  is  retained  in  these  isolated 
somatic  cells.  H.  V.  "Wilson  has  shown  that  in  coelenter- 
ates  and  sponges  complete  new  individuals  may  develop 
in  vitro  from  isolated  cells  taken  from  adult  animals. 
By  squeezing  small  bits  of  these  animals  through  bolting 
cloth  he  was  able  to  separate  small  groups  of  cells  or 
even  single  cells.  In  culture  these  would  grow  into  small 
masses  of  cells  which  would  then  differentiate  slowly  into 
the  normal  form  of  the  complete  organism.  Figure  16 
shows  an  example  of  this  taken  from  Wilson's  work. 

It  was  early  demonstrated  by  Carrel  and  Burrows 
that  the  life  of  the  tissues  in  vitro,  which  varied  in  differ- 
ent experiments  from  5  to  20  days,  could  be  prolonged  by 
a  process  of  successive  transfers  of  the  culture  to  an 
indefinite  period.  Cells  which  were  nearing  the  end  of 
their  life  and  growth  in  one  culture  need  only  be  trans- 
ferred to  a  new  culture  medium  to  keep  on  growing  and 
multiplying.  Dr.  and  Mrs.  Warren  H.  Lewis  made  the 
important  discovery  that  tissues  of  the  chick  embryo 
could  be  cultivated  outside  the  body  in  purely  inorganic 
solutions,  such  as  sodium  chloride,  Ringer's  solution, 
Locke's  solution,  etc.  No  growth  in  these  inorganic  cul- 
tures took  place  without  sodium  chloride.  Growth  was 
prolonged  and  increased  by  adding  calcium  and  potas- 
sium. If  maltose  or  dextrose,  or  protein  cleavage  pro- 
ducts were  added  proliferation  of  the  cells  increased. 

By  the  method  of  transfer  to  fresh  nutrient  media. 
Carrel  has  been  able  to  keep  cultures  of  tissue  from  the 
heart  of  the  chick  embryo  alive  for  a  long  period  of 
years.     In  a  letter,  recently  received,  he  says:     *^The 


Yjc,    If).— Ptniuuia.     Kcstituti.ni  muss  six  days  old.  completely  metamorphosed.  «ith 
developed  hydrantlis.     Op.  perisarc  ot  original  mass;  x,  perisarc  of  outgrowth  adherent  to 

glass.     (From  VV  ilson.) 


Fig.  17. — Culture  of  old  strain  of  connective  tissue.     1614  passage.      8  years  and  S  months  old, 
lacking  2  days.     48  hours'  growth.     x20.     (Ebeling). 


CONDITIONS  OF  CELLULAR  IMMORTALITY  G3 

strain  of  connective  tissue  obtained  from  a  piece  of  cliick 
heart  is  still  alive,  and  will  be  nine  years  old  the  seven- 
teenth of  January,  1921.''  Figure  17  is  a  photograph 
showing  the  present  condition  of  this  culture.  It  should 
be  understood  that  this  long  continued  culture  has  gone 
on  at  body  temperature  in  an  incubator,  and  not  by  keep- 
ing the  culture  at  a  low  temperature  and  merely  slowing 
down  the  vital  processes. 

Tliis  is  indeed  a  remarkable  result.  It  completes  the 
demonstration  of  the  potential  immortality  of  somatic 
cells,  when  removed  from  the  body  to  conditions  which 
permit  of  their  continued  existence.  Somatic  cells  have 
lived  and  are  still  living  outside  the  body  for  a  far  longer 
time  than  the  normal  duration  of  life  of  -the  species  from 
which  they  came.  I  think  the  present  extent  of  Carrel's 
cultures  in  time  fully  disposes  of  Harrison's  criticism 
to  the  effect  that  we  are  ^^not  justified  in  referring  to 
the  cells  as  potentially  immortal  or  even  in  spealdng 
of  the  prolongation  of  life  by  artificial  means,  at  least 
not  until  we  are  able  to  keep  the  cellular  elements  alive 
in  cultures  for  a  period  exceeding  the  duration  of  life 
of  the  organism  from  which  they  are  taken.  There  is 
at  present  no  reason  to  suppose  this  cannot  be  done,  but 
it  simply  has  not  been  done  as  yet."  I  have  had  many 
years'  experience  with  the  domestic  fowl,  and  have  par- 
ticularly studied  its  normal  duration  of  life,  and  discus- 
sed the  matter  vnth.  competent  observers  of  poultry.  I 
am  quite  sure  that  for  most  breeds  of  domestic  poultry 
the  normal  average  expectation  of  life  at  hirth  is  not 
substantially  more  than  two  years.  For  the  longest 
lived  races  we  know  this  normal  average  expectation 
of  life  cannot  be  over  four  years.  I  have  never  been  able 
to  keep  a  Barred  Plymouth  Rock  alive  more  than  seven 


64  BIOLOGYl  OF  DEATH 

years.  There  are  on  record  instances  of  fowls  living  to 
as  many  as  20  years  of  age.  But  these  are  wholly  excep- 
tional instances,  unquestionably  far  rarer  than  the  occur- 
rence of  centenarians  among  human  beings.  There  can 
be  no  question  that  the  nine  years  of  life  of  Carrel's 
culture  has  removed  whatever  validity  may  have  origin- 
ally inhered  in  Harrison's  point.  And  further  the  cul- 
ture is  just  as  vigorous  in  its  grqwth  today  as  it  ever 
was,  and  gives  every  indication  of  being  able  to  go  on 
indefinitely,  for  20  or  40,  or  any  desired  number  of  years. 
The  potential  immortality  of  somatic  cells  has  been 
logically  just  as  fully  demonstrated  in  another  way  as 
it  has  by  these  tissue  cultures.  Some  nineteen  years  ago, 
Leo  Loeb  first  announced  the  important  discovery  that 
potential  immortality  of  somatic  cells  could  be  demon- 
strated through  tumor  transplantations.  His  latest  sum- 
mary of  this  work  may  well  be  quoted  here : 

"We  must  remember  that  common,  transplantable  tumors  are  the  direct 
descendants  of  ordinary  tissue  cells,  such  as  we  normally  find  in  the 
individuals  of  the  particular  species  which  we  use.  The  tumors  may  be 
derived  from  a  variety  of  normal  tissues  and,  in  general,  the  transfor- 
mation from  normal  cells  into  tumor  cells  takes  place  under  the  influence 
of  a  long  continued  action  of  various  factors  enhancing  growth.  Tumor  cells 
are,  therefore,  merely  somatic  cells  which  have  gained  an  increased  growth 
energy  and  at  the  same  time  somehow  gained,  in  some  cases,  the  power  to 
escape  the  destructive  consequences  of  homoiotoxins.  This  ability  of  cer- 
tain tumors  to  grow  in  other  individuals  of  the  same  species  has  enabled 
us  to  prove,  through  apparently  endless  propagation  of  these  tumor  cells 
in  other  individuals,  that  ordinary  somatic  cells  possess  potential  im- 
mortality in  the  same  sense  in  which  protozoa  and  germ  cells  possess 
immortality.  Thus  tumor  transplantation  made  possible  the  establishment 
of  a  fact  of  great  biological  interest,  which,  because  of  the  homoiosensitive- 
ness  of  normal  tissues,  could  not  be  shown  in  the  latter. 

"We  wish,  however,  especially  to  emphasize  the  fact  that  our  experi- 
ments did  not  merely  prove  the  immortality  of  tumor  cells,  but  of  the 
ordin;ary  tissue  cells  as  well,  the  large  majority  or  all  of  which  can  be 
transformed   into  tumor   cells.     At  an  early  stage  of   our    investigations 


CONDITIONS  OF  CELLULAR  IMMORTALITY  05 

we  drew,  therefore,  on  the  basis  of  these  experiments,  the  conclusion  that 
ordinary  tissue  cells  are  potentially  immortal;  notwithstanding  the  fact 
that,  especially  under  Weismann's  influence,  the  opposite  view  had  been 
generally  accepted,  and  as  it  seems  to  us,  with  full  justification,  inasmuch 
as  no  facts  were  known  at  that  time  which  suggested  the  immortality 
of  somatic  cells.  It  was  the  apparently  endless  transplantation  of  tumor 
cells  which  proved  the  contrary  view, 

"To  recapitulate  what  we  stated  above :  tumors  are  merely  transformed 
tissue  cells.  All  or  the  large  majority  of  adult  tissues  are  potential  tumor 
cells.  Tumor  cells  have  been  shown  experimentally  to  be  potentially  im- 
mortal, therefore  tissue  cells  are  potentially  immort^al. 

"  This  wider  conclusion  I  expressed  nineteen  years  ago.  Quite  recently, 
the  immortality  of  certain  connective  tissue  cells  has  been  demonstrated 
by  Carrel  through  in  vitro  culture  of  these  cells.  Under  those  conditions 
the  tissue  cells  escape  the  mechanisms  of  attack  to  which  the  homoiotoxins 
expose  the  ordinary  tissue  cells  in  other  individuals  of  the  same  species. 
Under  these  conditions  the  reactions  of  the  host  tissue  against  homoiotoxins 
which  would  have  taken  place  in  vivo,  are  eliminated.  We  must,  however, 
keep  in  mind  that  this  method  of  proving  the  immortality  of  somatic  cells 
applies  only  to  one  particular,  very  favorable  kind  of  cells;  and  it  is  very 
doubtful,  if,  by  cultivation  in  vitro,  the  same  proof  could  be  equally  well 
supplied  in  the  case  of  other  tissues.  On  the  basis  of  tumor  transplanta- 
tions, on  the  contrary,  we  were  able  to  show  that  a  considerable  variety, 
perhaps  the  large  majority  of  all  tissue  cells  possess  potential  immortality." 

To  Loeb  unquestionably  belongs  the  credit  for  first 
perceiving  that  death  was  not  a  necessary  inlierent  con- 
sequence of  life  in  the  somatic  cell,  and  demonstrating  by 
actual  experiments  that  somatic  cells  could,  under  cer- 
tain conditions,  go  on  living  indefinitely. 

Before  turning  to  the  next  phase  of  our  discussion, 
let  us  summarize  the  ground  we  have  covered  up  to  this 
point.  We  have  seen  that  by  appropriate  control  of 
conditions,  it  is  possible  to  prolong  the  life  of  cells  and 
tissues  far  beyond  the  limits  of  longevity  to  wliich  they 
would  attain  if  they  remained  in  the  multicellular  body 
from  which  they  came.  Tliis  is  true  of  a  wide  variety 
of  cells  and  tissues  differentiated  in  various  ways.  In- 
deed, the  range  of  facts  which  have  been  ascertained 

5 


66  EIOLCGY  OF  DEATH 

by  experimental  work  in  this  field,  probably  warrants 
the  conclusion  that  this  potential  longevity  inheres  in 
most  of  the  different  kinds  of  cells  of  the  metazoan  body, 
except  those  which  are  extremely  differentiated  for  par- 
ticular functions.  To  bring  this  potential  immortality 
to  actuality  requires,  of  course,  special  conditions  in 
each  particular  case.  Many  of  these  special  conditions 
have  already  been  discovered  for  particular  tissues  and 
particular  animals.  Doubtless,  in  the  future  many  more 
will  be  worked  out.  We  have  furthermore  seen  that  in 
certain  cases  the  physico-chemical  nature  of  the  condi- 
tions necessary  to  insure  the  continuance  of  life  has  been 
definitely  worked  out  and  is  well  understood.  Again 
this  warrants  the  expectation  that,  Avitli  more  extended 
and  penetrating  investigations  in  a  field  of  research 
which  is  really  just  at  its  beginning,  we  shall  understand 
the  physics  and  chemistry  of  prolongation  of  life  of  cells 
and  tissues  in  a  great  many  cases  where  now  we  know 
nothing  about  it. 

One  further  point  and  we  shall  have  done  with  this 
phase  of  our  discussion.  The  experimental  culture  of 
cells  and  tissues  in  vitro  has  now  covered  practically  all 
the  essential  tissue  elements  of  the  metazoan  body,  even 
including  the  most  highly  differentiated  of  those  tissues. 
Nerve  cells,  muscle  cells,  heart  muscle  cells,  spleen  cells, 
connective  tissue  cells,  epithelial  cells  from  various  loca- 
tions in  the  body,  kidney  cells,  and  others  have  all  been 
successfully  cultivated  in  vitro.  We  may  fairly  say,  I  be- 
lieve, that  the  potential  immortality  of  all  essential  cel- 
lular elements  of  the  body  either  has  been  fully 
demonstrated,  or  else  has  been  carried  far  enough  to 
make  the  probability  very  great  that  properly  conducted 
experiments  would  demonstrate  the  continuance  of  the 


CONDITIONS  OF  CELLUL.\R  IMMORTALITY  67 

life  of  these  cells  in  culture  to  any  definite  extent.  It 
is  not  to  be  expected,  of  course,  that  such  tissues  as  hair, 
or  nails,  would  be  capable  of  independent  life,  l)ut  these 
are  essentially  unimportant  tissues  in  the  animal  econ- 
omy as  compared  with  those  of  the  heart,  the  nervous 
system,  the  kidneys,  etc.  What  I  am  leading  to  is  the 
broad  generalization,  perhaps  not  completely  demon- 
strated yet,  but  having  regard  to  Leo  Loeb's  work,  so 
near  it  as  to  make  little  risk  inhere  in  predicting  the 
final  outcome,  that  all  the  essential  tissues  of  the  meta- 
zoan  body  are  potentially  immortal.  The  reason  that 
they  are  not  actually  immortal,  and  that  multicellular 
animals  do  not  live  forever,  is  that  in  the  differentiation 
and  specialization  of  function  of  cells  and  tissues  in  the 
body  as  a  whole,  any  individual  part  does  not  find  the 
conditions  necessary  for  its  continued  existence.  In 
the  body  any  part  is  dependent  for  the  necessities  of  its 
existence,  as  for  example  nutritive  material,  upon  other 
parts,  or  put  in  another  way,  upon  the  organization  of 
the  body  as  a  whole.  It  is  the  cliff ereyitiation  and  spe- 
cialization of  function  of  the  mutually  dependent  aggre- 
gate of  cells  and  tissues  ivhich  constitute  the  metazoan 
body  ivhich  brings  about  deaths  and  not  any  inherent  or 
inevitable  mortal  process  in  the  individual  cells  them- 
selves. 

An  examination  of  different  lines  of  evidence  has 
led  us  to  two  general  conclusions,  viz: 

a.  That  the  individual  cells  and  tissues  of  the  body, 
in  and  by  themselves,  are  potentially  immortal. 

b.  That  death  of  the  metazoan  l)ody  occurs,  funda- 
mentally, because  of  the  way  in  which  the  cells  and  tis- 
sues are  organized  into  a  mutually  dependent  system. 

Is  there  any  further  and  direct  evidence  to  be  liad 


68  BIOLOGY  OF  DEATH 

■apon  the  second  of  these  conclusions?  So  far  our  evi- 
dence in  its  favor  has  been  indirect  and  inferential, 
though  cogent  so  far  as  it  goes.  In  this  connection,  a 
paper  of  FriedenthaPs  is  of  considerable  interest.  He 
shows  that  there  is  a  marked  correspondence  between  the 
longevity  of  various  species  of  animals  and  a  constant 
of  organization  which  he  calls  the  ^^cephalisation  factor. '^ 
This  cephalisation  factor  in  pure  form,  in  his  sense,  is 
given  by  the  equation. 

^     ,    ,.    *•      r    4.  Brain  weight 

Cephalisation  factor  =  ^  ^  , >  u  j 1 — ^ 

^  Total  mass  of  body  pT-otoplasm, 

Now  ^Hotal  mass  of  body  protoplas^n,^^  as  distinct  from 
supporting  structures,  such  as  bone  etc.,  is  obviously 
difficult  to  determine  directly.  But  Friedenthal  is  well 
convinced  that,  to  a  first  approximation,  the  cephalisa- 
tion factor  may  be  written  in  this  way: 

^    ,    ,.     ,.      ,     ,  Brain  weight 

Cephalisation  factor  =  .^    , r-r-t  ^ 

^  (Body  weight) 

Computed  upon  the  latter  basis  he  sets  up  tables  of  the 
relation  between  cephalisation  factor  and  longevity  for 
mammals  and  for  birds.  It  is  not  necessary  to  repro- 
duce here  the  long  tables,  but  to  show  the  general  point, 
the  following  table  for  five  selected  species  of  mammals 
will  suffice: 

TABLE  5 

Relation  between  the  cephalisation  factor  and  longevity  (Friedenthal) 


Species 

Cephalisation  index 

Duration  of  life 

Muuse 

0.045 

6  years 

Rabbit 

.066 

8  years 

Marmoset  (Callithrix) 

.216 

12  years 

Deer 

.35 

15  years 

Man 

2.7 

100  years 

There  appears  in  this  short  selected  table  a  defect 


CONDITIONS  OF  CELLULAR  IMMORTALITY  69 

which  is  even  more  apparent  in  his  long  ones,  namely, 
that  the  figures  for  duration  of  life  are  distinctly  round 
numbers.  There  is  no  evidence,  for  example,  that  the 
normal  life  span  of  the  mouse  is  6  years.  All  who  have 
statistically  studied  the  matter  agree  upon  a  much  smal- 
ler figure  than  this.  But,  leaving  this  point  aside,  it  is 
apparent  that  there  is  a  parallelism  of  striking  sort  be- 
tween the  cephalisation  factor  and  duration  of  life.  In 
other  words,  it  appears  that  the  manner  in  which  higher 
vertebrates,  at  least,  are  put  together  in  respect  of  the 
proportionality  of  brain  and  body  is  markedly  associated 
with  the  duration  of  life.  It  would  be  a  matter  of  great 
interest  to  see  whether  this  correlation  between  relative 
brain-weight  and  the  expectation  of  life  holds  intra- 
racially  as  well  as  it  does  inter-racially.  The  bearing  of 
these  results  of  Friedenthal's  upon  our  results  as  to  the 
distribution  of  mortality  upon  a  germ-layer  basis,  to  be 
discussed  in  Chapter  V  infra,  is  obvious. 

Another  possible  illustration  of  the  general  point 
now  under  discussion  may  be  found  in  some  recent  work 
of  Robertson  and  Ray.  These  authors,  in  a  recent  paper, 
have  analyzed  the  growth  curves  of  relatively  long-lived 
mice  as  compared  with  the  curves  shown  by  relatively 
short-lived  individuals.  In  the  experiment  both  groups 
were  subjected  to  the  same  kind  of  experimental  treat- 
ment of  various  sorts,  and  the  care  with  which  the  experi- 
ments were  conducted  in  respect  of  control  of  the 
environmental  factors  renders  the  results  highly  inter- 
esting and  valuable.  The  long-lived  animals  form  a  group 
which  grows  more  rapidly  in  early  life,  and  at  the  same 
time  is  less  variable  than  the  short  lived  group.  The 
short-lived  animals  often  grow  much  more  rapidly  in 
later  life  than  the  long-lived,  but  this  accretion  of  tissue 


70  BIOLOGY  OF  DEATH 

was  found  to  be  relatively  unstable..  They  further  found 
that  the  long-lived  animals  represent  a  relatively  stable 
group,  highly  resistant  to  external  disturbing  factors, 
and  showing  a  more  or  less  marked  but  not  invariable 
tendency  to  early  overgro\\i:h  and  relative  paucity  of 
tissue  accretion  in  late  life.  The  short-lived  animals  are 
on  the  contrary  relatively  unstable,  sensitive  to  external 
disturbing  factors,  and,  as  a  rule,  but  not  invariably,  dis- 
play relatively  deficient  early  growth  and  a  tendency  to 
rapid  accretion  of  tissue  in  later  life. 

In  interpreting  these  results,  Robertson  and  Ray  be- 
lieve that  the  differences  are  based  upon  the  fact  that 
in  early  or  embryonic  life  the  outstanding  characteristic 
of  the  tissues  is  a  high  proportion  of  cellular  elements, 
whereas  in  old  age  there  is  a  marked  increase  in  connective 
tissues.  They  further  point  out  that  connective  tissue 
elements  are  ultimately  dependent  upon  cellular  tissues 
for  their  support,  and  that  the  comiective  tissues  are 
expensive  to  maintain.  They  believe  that  the  reason  that 
the  substance  tethelin  (cf.  Chap.  VII  infra)  prolongs  life 
is  because  it  accelerates  the  metabolism  of  the  cellular 
elements  to  the  detriment  of  the  connective  tissue  ele- 
ments. Longe\dty  on  this  view  is  determined  not  by  the 
absolute  mass  of  living  substance,  but  by  the  relative 
proportions  of  parenchymatous  to  sclerous  tissues. 

SENESCENCE 

The  facts  presented  in  this  and  the  preceding  chapter 
clearly  make  it  necessary  to  review  with  some  care  the 
current  conception  of  senescence.  Senescence,  or  grow- 
ing old,  is  commonly  considered  to  be  the  necessary  prel- 
ude to  "natural,''  as  distinguished  from  accidental  death. 


CONDITIONS  OF  CELLULAR  IMMORTALITY  71 

But  is  the  evidence  really  sound  and  complete  that  such 
is  the  fact? 

A  careful  and  unprejudiced  examination  will  inevi- 
tably suggest  to  the  open  mind,  I  think,  that  much  of  the 
existing  literature  on  senescence  is  really  of  no  funda- 
mental importance,  because  it  has  unwittingly  reversed 
the  true  sequential  order  of  the  causal  nexus.  If  cells 
of  nearly  every  sort  are  capable,  under  appropriate  con- 
ditions, of  living  indefinitely  in  undiminished  vigor,  and 
cytological  normality,  there  is  little  ground  for  postu- 
lating that  the  observed  senescent  changes  in  these  cells 
while  in  the  body,  such  as  those  described  by  Minot  and 
others,  are  expressive  of  specific  and  inherent  mortal 
processes  going  on  in  the  cells ;  or  that  these  cellular  pro- 
cesses are  the  cause  of  senescence,  as  Minot  has  concluded. 

That  there  is  such  a  phenomenon  as  senescence  is,  of 
course,  certain.  It  is  observable  both  in  Protozoa  and 
in  Metazoa.  The  real  question,  however,  is  a  twofold 
one,  viz:  (a)  is  senescence  in  either  Protozoa  or  Metazoa 
an  inevitable  consequence  of  the  strain  or  the  individual 
having  lived;  and  (b)  is  senescence  a  necessary  asso- 
ciate and  forerunner  of  natural  death? 

Let  us  briefly  reconsider  the  facts.  In  Protozoa  a 
slowing  down  of  the  division  rate  in  culture  has  been 
frequently  observed;  and  it  has  been  held,  first,  that 
this  is  a  phenomenon  essentially  homologous  to  senes- 
cence in  the  metazoan;  and  second,  that  if  nuclear 
reorganization,  by  the  way  either  of  endomixis  or  of 
conjugation,  did  not  occur  that  the  strain  would  die  out. 
Indeed,  Jennings,  in  discussing  the  matter  in  his  last 
book  says: 

"Thus  it  appears  that  in  these  organisms  nature  has  employed  the 
method   of   keeping   on    hand   a    reserve    stock    of   a   material    essential    to 


72  BIOLOGY  OF  DEATH 

life;  by  replacing  at  intervals  the  worn  out  material  with  this  reserve, 
the  animals  are  kept  in  a  state  of  perpetual  vigor;  not,  as  individuals, 
growing  old  or  dying  a  natural  death.  Nevertheless,  a  wearing  out  pro- 
cess, such  as  might  be  called  getting  old,  does  occur  in  the  structures 
employed  in  the  active  functions  of  life,  and  these  must  be  replaced  after 
a  time  of  service.  So  far  as  the  conditions  in  these  organisms  are  typical, 
deterioration  and  death  do  appear  to  be  a  consequence  of  full  and  active 
life;  life  carries  within  itself  the  seeds  of  death.  It  is  not  mating  with 
another   individual   that   avoids   this   end;    but   replacement  of   the  worn 

material  by  a  reserve The  great  mass  of  cells  subject  to  death  in  the 

higher  animals  dwindles  in  the  infusorian  to  the  macronucleus ;  this  alone 
represents  a  corpse.  But  the  dissolution  of  this  corpse  occurs  within 
the  living  body.  It  much  resembles  such  a  process  as  the  wasting  away 
and  destruction  of  minute  parts  of  our  own  bodies,  which  we  know  is 
taking  place  at  all  times,  and  which  does  not  interrupt  the  life  of 
the  individual." 

It  is  doubtful  if  this  position  is  warranted.  Since 
Jennings  wrote  the  statement  quoted,  some  new  and 
pertinent  data  have  appeared  in  regard  to  amicronu- 
cleate  infusoria.  Woodruff  and  his  co-rWorkers  have 
shown  that  such  races  may  occur  rather  commonly.  Thus 
Woodruff,  in  1921,  says: 

"During  the  past  year,  the  isolation  for  certain  experiments  of  14 
"wild"  lines  representing  6  species  of  hypotrichous  ciliates  revealed  7  lines 
(4  species)  with  micronuclei  and  7  lines  (2  species)  without  morphological 
micronuclei.  Ten  of  the  lines  were  all  isolated  from  a  "wild"  mass  culture 
of  the  same  species  Urostyla  grandis,  found  in  a  laboratory  aquarium. 
Six  of  these  lines  were  amicronucleate.  All  of  the  lines  of  all  of  the 
species  have  bred  true  with  respect  to  the  character  in  question,  and  one 
amicronucleate  line  at  present  is  at  the  102d  generation. 

Similarly  a  culture  of  Paramecium  caudatum,  which  the  present  writer 
supplied  a  year  ago  to  a  course  in  protozoology  for  the  study  of  the  nucleus, 
failed  to  reveal  a  micronucleus,  although  in  other  races  the  micronucleus 
was  readily  demonstrated." 

Now,  since  it  is  the  micronucleus  which  furnishes  for 
the  process  of  endomixis  the  **  reserve  stock  of  a  material 
essential  to  life"  which  Jennings  discusses,  it  is  plain 
that  the  existence  of  amicronucleate  races  of  Protozoa 


CONDITIONS  OF  CELLULAR  IMMORTALITY  73 

at  once  puts  a  new  face  upon  the  whole  matter.  Dawson 
has  studied  in  continued  culture  one  of  these  amicronu- 
cleate  races  of  Oxytriclia  hymenostoma  Stokes.  His  con- 
clusion is  as  follows : 

"The  existence  of  a  form  which  not  only  apparently  may  live  indefi- 
nitely without  conjugation,  autogamy,  or  endomixis  (assuming  the  possi- 
bility  of  the  latter  phenomenon  in  an  hypotrichoua  form),  but  also 
apparently  does  not  possess  the  ability  to  undergo  any  of  these  phenomena, 
brings  to  light  an  entirely  new  possibility  in  the  life  history  of  ciliates. 
It  has  been  proved  quite  conclusively,  (WoodrufiF,  '14),  that  in  forms 
which  ordinarily  conjugate,  the  continued  prevention  of  this  process  brings 
about  no  loss  of  viability  if  a  favorable  environment  be  provided.  How- 
ever, in  the  organism  under  consideration  there  is  apparently  no  possi- 
bility not  only  of  conjugation  or  endomixis,  but  also  of  autogamy;  and 
thus  we  have  from  another  source  crucial  evidence  that  none  of  these 
phenomena  is  an  indispensable  factor  in  the  life-history  of  this  hypo- 
trichous  form." 

In  the  light  of  these  clean  cut  and  definite  results 
one  is  more  disposed  than  was  formerly  the  case  to 
accept  at  their  face  value  the  results  of  Enriques  \vith 
Glaucoina  pyriformiSj  and  those  of  Hartmann  with 
Eudorina  elegans,  in  which  reproduction  went  on  indef- 
initely with  undiminished  vigor  and  no  e\^dence  of  any 
process  comparable  to  endomixis. 

Altogether,  it  seems  to  me  that  the  weight  of  the  evi- 
dence now  is  that  in  the  Protozoa,  senescence  (or  deatli), 
is  not  a  necessary  or  inevitable  consequence  of  life. 
Given  the  appropriate  and  necessary  conditions  of  envi- 
ronment, true  immortality — the  absence  of  both  senes- 
cence and  natural  death,  each  defined  in  the  most  critical 
manner — is  in  fact  the  reality  for  a  number  of  forms. 

Turning  to  the  metazoan  side  of  the  case,  the  evidence 
regarding  senescence  is  equally  cogent.  In  the  first  place, 
in  the  longest  continued  in  vitro  tissue  cultures  known 
(those  of  Carrel)  there  is,  as  already  stated,  no  appear- 


74  BIOLOGY  OF  DEATH 

ance  of  senescence  in  the  cells.  But  it  may  be  objected 
that  an  element  of  uncertainty  is  injected  into  the  case, 
by  the  fact  that,  as  Carrel  and  Ebeling  have  lately  dis- 
cussed in  some  detail,  it  has  been  necessary  in  carrying 
along  this  long-continued  culture  to  add  regularly  to  the 
culture  medium  a  small  amount  of  ** embryonic  juice.'* 
One  might  urge  that,  but  for  the  *  *  embryonic  juice, ' '  cellu- 
lar senescence  and  death  would  have  appeared.  But 
suppose  this  to  be  granted  fully.  It  does  not  mean 
that  senescence  is  a  necessary  and  inevitable  consequence 
of  life,  but  only  that  to  realize  a  potential  immortality 
the  cells  must  have  an  appropriate  environment,  one 
element  of  which  is  presumably  some  chemical  combination 
which,  so  far,  one  has  supplied  only  through  **  embry- 
onic juice." 

An  entirelv  different  sort  of  evidence  and  one  of 
great  significance  is  found  in  the  facts  of  clonal  propaga- 
tion of  plants,  well  known  to  horticulturists.  An  individ- 
ual apple  tree  grows  old,  and  eventually  dies,  as  a  tree. 
But  at  all  periods  of  its  life,  including  all  stages  of 
senescence  up  to  the  terminal  one,  death,  it  produces 
shoots  each  spring.  If  one  of  these  shoots  is  grafted  to 
another  root,  it  will,  in  the  passage  of  time,  make  first 
a  young  tree,  then  a  middle  aged  tree,  and  finally  an  old, 
senescent  tree;  which,  in  turn,  will  make  new  shoots, 
which  may,  in  turn,  be  grafted  to  new  roots,  and  so  on 
ad  infinitum.  It  is  not  even  absolutely  necessary  that 
the  shoot  be  grafted  to  a  new  root;  though,  of  course, 
this  is  the  manner  in  which  the  great  majority  of  our 
orchards  are,  in  fact,  propagated,  and  have  been  since 
the  beginning  of  horticultural  history.  Anyone  who  is 
familiar  wdth  the  woods  of  New  England,  not  too  far  from 
settlements,  has  seen  apple  trees  in  the  woods  where  a 


CONDITIONS  OF  CELLULAR  IMMORTALITY  75 

shoot,  whose  continuity  with  the  base  of  its  parent  tree 
has  never  been  broken,  makes  a  new  tree  after  the  okl  one 
has  died— indeed  in  some  cases  the  shoot  has  lielped  the 
mortiferous  process  by  the  vigorous  crowding  of  youth. 
In  tliis  whole  picture  how  fares  any  idea  of  the  necessity 
or  inevitahleness  of  cellular  (somatic)  senescence?  Such 
an  idea  plainly  has  no  place  in  the  realities  of  the  con- 
tinued existence  of  apple  trees. 

From  these  facts  it  is  a  logically  cogent  induction  to 
infer  that  when  cells  show  the  characteristic  senescent 
changes  which  were  discussed  in  the  preceding  chapter, 
it  is  because  they  are  reflecting  in  their  morphology  and 
physiology  a  consequence  of  their  mutually  dependent 
association  in  the  body  as  a  whole,  and  not  any  necessary 
progressive  process  inherent  in  themselves.  In  other 
words,  may  we  not  tentatively,  in  the  light  of  our  present 
knowledge,  regard  senescence  as  a  phenomenon  appear- 
ing in  the  ynulticellular  body  as  a  whole,  as  a  result  of 
the  fact  that  it  is  a  differentiated  and  conferentiated  (to 
employ  a  useful  term  lately  introduced  by  Ritter)  mor- 
phologic and  dynamic  orgayiization,  Tliis  phenomenon 
is  reflected  morphologically  in  the  component  cells.  But 
it  does  not  primarily  originate  in  any  particular  cell 
because  of  the  fact  that  that  cell  is  old  in  time,  or  because 
that  cell  in  and  of  itself  has  been  alive ;  nor  does  it  occur 
in  the  cells  when  they  are  removed  from  the  mutually 
dependent  relationship  of  the  organized  body  as  a 
whole  and  given  appropriate  physico-chemical  condi- 
tions. In  short,  senescence  appears  not  to  be  a  primary 
attribute  of  the  physiological  economy  of  cells  as  such. 

If  tliis  conception  of  the  phenomenon  of  senescence 
is  correct  in  its  main  features,  it  suggests  the  essential 
futility  of  attempting  to  investigate  its  causes  by  purely 


76  BIOLOGY  OF  DEATH 

cytological  methods.  On  the  other  hand,  by  clearing 
away  the  unessential  elements,  it  indicates  where  research 
into  the  problem  of  causation  of  senescence  may  be 
profitable. 

An  extremely  interesting  contribution  to  the  problem 
of  senescence  has  been  made  by  Carrel  and  Ebeling  in 
their  most  recent  paper,  in  which  they  show  that  the  rate 
of  multiplication  of  fibroblasts  in  vitro,  and  the  duration 
of  life  of  such  cultures,  is  inversely  proportional  to  the 
age  of  the  animal  from  which  the  serum  for  the  culture 
medium  is  taken.  These  results  are  of  such  considerable 
interest  that  it  will  be  well  to  quote  in  full  the  summary 
of  them  given  by  the  authors: 

"Pure  cultures  of  fibroblasts  displayed  marked  differences  in  their 
activity  in  the  plasma  of  young,  middle  aged,  and  old  chickens.  The  rate 
of  cell  multiplication  varied  in  inverse  ratio  to  the  age  of  the  animal  from 
which  the  plasma  was  taken.  There  was  a  definite  relation  between  the 
age  of  the  animal  and  the  amount  of  new  tissue  produced  in  its  plasma 
in  a  given  time.  The  chart  obtained  by  plotting  the  rate  of  cell  prolifera- 
tion in  ordinates,  and  the  age  of  the  animal  in  abscissae,  showed  that  the 
rate  of  growth  decreased  more  quickly  than  the  age  increased.  The  de- 
crease in  the  rate  of  growth  was  50  per  cent,  during  the  first  3  years  of 
life,  while  in  the  following  6  years  it  was  only  30  per  cent.  When  the 
duration  of  the  life  of  the  cultures  in  the  four  plasmas  was  compared,  a 
curve  was  obtained  which  showed  about  the  same  characteristics.  The 
duration  of  life  of  the  fibroblasts  in  vitro  varied  in  inverse  ratio  to  the 
age  of  the  animal,  and  decreased  more  quickly  than  the  age  increased. 

'*As  the  differences  in  the  amount  of  new  tissue  produced  in  the 
plasma  of  young,  middle  aged,  and  old  chickens  were  large,  the  growth 
of  a  pure  culture  of  fibroblasts  could  be  employed  as  a  reagent  for  detect- 
ing certain  changes  occurring  in  the  plasma  under  the  influence  of  age. 

"  A  comparative  study  of  the  growth  of  fibroblasts  in  media  containing 
no  serum,  and  serum  under  low  and  high  concentrations  was  made,  in  order 
to  ascertain  whether  the  decreasing  rate  of  cell  multiplication  was  due  to 
the  loss  of  an  accelerating  factor,  or  to  the  increase  of  an  inhibiting  one. 
In  high  and  low  concentrations  of  the  serum  of  young  animals,  no  difi'erence 
in  the  rate  of  multiplication  of  fibroblasts  was  observed.  This  showed 
that  the  serum  of  an  actively  growing  animal  did  not  contain  any  accel- 


THE  CHANCES  OF  DEATH  77 

erating  agent.  The  same  experiments  were  repeated  with  the  serum  of 
a  3  year  old  and  a  9  year  old  chicken.  The  medium  made  of  a  hi^'h 
concentration  of  serum  had  a  markedly  depressing  eflect  on  the  growth, 
and  this  effect  was  greater  in  the  serum  of  the  older  animal. 

"The  results  of  the  experiments  showed  in  a  very  definite  manner  that 
certain  changes  occurring  in  the  serum  during  the  course  of  life  can  be 
detected  by  modifications  in  the  rate  of  growth  of  pure  cultures  of  fibro- 
blasts and  that  these  changes  are  characterized  by  the  increase  of  an 
inhibiting  factor,  and  not  by  the  loss  of  an  accelerating  one.  It  appeared, 
therefore,  that  the  substances  which  greatly  accelerate  the  multiplication 
of  fibroblasts  and  are  found  in  the  tissues  do  not  exist  in  the  blood  serum, 
or  are  constantly  shielded  by  more  active  inhibiting  factors.  The  curve 
which  expresses  the  variations  of  the  inhibiting  factor  in  function  of  the 
age  was  compared  with  that  showing  the  variations  of  the  rate  of  healing 
of  a  wound  according  to  the  age  of  the  subject.  For  wounds  of  equal  size, 
the  index  of  cicatrization,  which  expresses  the  rate  of  healing,  varies  in 
inverse  ratio  to  the  age.  The  different  values  of  the  index  of  cicatrization 
of  a  wound  40  sq.  cm.  in  area,  taken  from  measurements  made  by  du  Noiiy, 
were  plotted  in  ordinates,  and  the  age  of  the  subject  in  abscissae.  The 
curve  showed  a  decrease  in  the  activity  of  cicatrization,  which  resembled 
the  decrease  in  the  rate  of  growth  of  fibroblasts  in  function  of  the  age 
of  the  ianimal.  This  suggested  the  existence  of  a  relation  between  the 
factors  determining  both  phenomena." 

These  results  suggest  that  there  is  produced  in  some 
cases  by  the  body  or  some  of  its  parts,  a  substance 
which  inhibits  the  power  of  cells  to  multiply  or  to  remain 
alive.  How  general  such  a  phenomenon  is  in  occurrence 
does  not  yet  appear,  but,  apparently,  it  must  be  absent 
in  the  case  of  clonal  reproduction  in  plants  already  dis- 
cussed, and  in  the  analogous  case  of  agamic  reproduction 
in  lower  Metazoa  (cf,  planarians).  It  seems  possible 
that  the  results  of  Carrel  and  Ebeling  might  be  open  to 
a  slightly  different  interpretation  than  that  which  they 
give,  which  hypothecates  a  specific  inhibiting  substance 
in  the  serum,  increasing  in  either  amount  or  specific 
potency  with  age.  It  seems  to  me  that  all  of  their  facts 
could  be  interpreted  with  equal  cogency  on  the  supposi- 
tion that  the  serum  from  an  old  animal  is  itself  sencs- 


78  BIOLOGY  OF  DEATH 

cent  as  a  whole ;  that  is,  has  undergone  a  physico-chemi- 
cal alteration  (as  compared  with  that  of  a  young  ani- 
mal), which  is  comparable  to  the  morphological  and 
physiological  changes  which  are  observable  in  senescent 
cells.  It  may  further  quite  reasonably  be  supposed  that 
^^ senescent"  serum,  because  of  these  physico-chemical 
alterations,  does  not  furnish  so  favorable  a  nutrient  me- 
dium for  in  vitro  cultures  as  does  ^^young''  serum.  Such 
a  view  avoids  the  necessity  of  postulating  a  specific 
^^ senescent"  substance,  the  existence  of  which  would  be 
exceedingly  difficult  to  prove. 

But  in  any  case,  whatever  explanation  is  suggested 
for  Carrel  and  Ebeling's  brilliant  results,  it  does  not 
seem  to  me  that  the  results  themselves,  which  alone  are 
the  realities  pertinent  in  the  premises,  either  offer  any 
obstacle  to  or,  indeed,  alter  the  interpretation  of  senes- 
cence which  I  have  suggested  above.  For,  what  the  re- 
sults really  demonstrate  is,  essentially,  that  the  serum  of 
old  animals  is  a  less  favorable  component  of  the  nutrient 
medium  of  cells  in  vitro  than  is  the  serum  of  young  ani- 
mals. This  fact  is  a  contribution  to  our  knowledge  of 
the  phenomena  and  attributes  of  senescence  of  first-class 
importance ;  but  it  does  not  per  se,  as  it  appears  to  me, 
permit  of  any  new  generalization  as  to  the  etiology  of 
senescence. 


CHAPTER  III 
THE  CHANCES  OF  DEATH 

THE  LIFE   TABLE 

Up  to  this  point  in  our  discussion  of  death  and  lon- 
gevity we  have,  for  the  most  part,  dealt  with  general  and 
qualitative  matters,  and  have  not  made  any  particular 
examination  as  to  the  quantitative  aspects  of  the  prob- 
lem of  longevity.  To  this  phase  attention  may  now  be 
directed.  For  one  organism,  and  one  organism  only,  do 
we  know  much  about  the  quantitative  aspects  of  longevity. 
I  refer,  of  course,  to  man,  and  the  abundant  records  which 
exist  as  to  the  duration  of  his  life  under  various  condi- 
tions and  circumstances.  In  1532  there  began  in  London 
the  first  definitely  known  compilation  of  weekly  ''Bills 
of  Mortality.''  Seven  years  later,  the  official  registra- 
tion of  baptisms,  marriages  and  deaths  was  begun  in 
France,  and  shortly  after  the  opening  of  the  seventeentli 
century  similar  registration  was  begun  in  Sweden.  In 
1662  was  published  the  first  edition  of  a  remarkable  book, 
a  book  which  marks  the  beginning  of  the  subject  which  we 
now  know  as  ' '  vital  statistics. ' '  I  refer  to  ' '  Natural  and 
Political  Observations  Mentioned  in  the  Following  Index, 
and  made  upon  the  Bills  of  Mortality"  by  Captain  Julm 
Graunt,  Citizen  of  London.  From  that  day  to  this,  in 
an  ever  widening  portion  of  the  inhabited  globe  we  have 
had  more  or  less  continuous  published  records  about  the 
duration  of  life  of  man.  The  amount  of  such  material 
which  has  accumulated  is  enormous.     We  are  onlv  at  the 

79 


80  BIOLOGY  OF  DEATH 

beginning,  however,  of  its  proper  matliematical  and  bio- 
logical analysis.  If  biologists  had  been  furnished  with 
data  of  anything  like  the  same  quantity  and  quality  for 
any  other  organism  than  man  it  is  probable  that  a  vastly 
greater  amount  of  attention  would  have  been  devoted  to 
them  than  ever  has  been  given  to  vital  statistics,  so-called, 
and  there  would  have  been  as  a  result  many  fundamental 
advances  in  biological  knowledge  now  lacking,  because 
material  of  this  sort  so  generally  seems  to  the  profes- 
sional biologist  to  be  something  about  which  he  is  in  no 
way  concerned. 

Let  us  examine  some  of  the  general  facts  about  the 
normal  duration  of  life  in  man.  We  may  put  the  matter 
in  this  way :  Suppose  we  started  out  at  a  given  instant  of 
time  with  a  hundred  thousand  infants,  equally  distributed 
as  to  sex,  and  all  born  at  the  same  instant  of  time.  How 
many  of  these  individuals  would  die  in  each  succeeding 
year,  and  what  would  be  the  general  picture  of  the  changes 
in  this  cohort  with  the  passage  of  time?  The  facts  on  this 
point  for  the  Kegistration  Area  of  the  United  States  in 
1910  are  exhibited  in  Figure  18,  which  is  based  on 
Glover's  United  States  Life  Tables. 

In  tliis  table  are  seen  two  curved  lines,  one  marked  I  x 
and  the  other  dx.  The  Ix  line  indicates  the  number  of 
individuals,  out  of  the  original  100,000  starting  together 
at  birth,  who  survived  at  the  beginning  of  each  year  of 
the  life  span,  indicated  along  the  bottom  of  the  diagram. 
The  dx  line  shows  the  number  dying  within  each  year 
of  the  life  span.  In  other  words,  if  we  subtract  the  num- 
ber dying  within  each  year  from  the  number  surviving 
at  the  beginning  of  that  year  we  shall  get  the  series  of 
figures  plotted  as  the  h  line.  We  note  that  in  the  very 
first  year  of  life  the  original  hundred  thousand  lose  over 


THE  CHANCES  OF  DEATH 


81 


one-tenth  of  their  number,  there  being  only  88,538  sur- 
viving at  the  beginning  of  the  second  year  of  life.  In 
the  next  year  2,446  drop  out,  and  in  the  year  following 
that  1,062.  Then  the  line  of  survivors  drofjs  off  more 
slowly  between  the  period  of  youth  and  early  adult  life. 
At  40  years  of  age,  almost  exactly  30,000  of  the  original 
100,000  have  passed  away,  and  from  that  point  on  the  / , 
line  descends  with  ever  increasing  rapidity,  until  about 


90.OCC 

^ 

MILL 

3     SI 

■ATCS 

ur 

C        T 

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-     fi 

MO 

eoooc 





^ 

^ 

H 

— 

\ 

\. 

M£>OC> 



\ 

\ 

\ 

iCOOO 

\ — 

\ 

V 

A- 

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\ 

\ 

b; 

ilo  ti  X> 


.\3  60  a? 


vLA^s   01  urc 


FiQ.  18. — Life  table  diagram.     For  explanation  see  text. 

age  80,  when  it  once  more  begins  to  drop  more  slowly, 
and  the  last  few  survivors  pass  out  gradually,  a  few  each 
year  until  something  over  the  century  mark  is  reached, 
when  the  last  one  of  the  100,000  who  started  across  the 
bridge  of  life  together  will  have  ended  his  journey. 

This  diagram  is  a  graphic  representation  of  that  im- 
portant type  of  document  knowai  as  a  life  or  mortality 
table.  It  puts  the  facts  of  mortality  and  longevity  in  their 
best  form  for  comparative  purposes.  The  first  such 
table  actually  to  be  computed  in  anytliing  like  the  modern 
fashion  was  made  by  the  astronomer.  Dr.  E.  Ilalley,  and 

6 


82  BIOLOGY  OF  DEATH 

was  published  in  1693,  although  thirty  years  before  that 
time  Pascal  and  Fermat  {cf.  Levasseur)  had  laid  down 
certain  mathematical  rules  for  the  calculation  of  the 
probabilities  of  human  life.  Since  Halley's  time  a  great 
number  of  such  tables  have  been  calculated.  Dawson 
fills  a  stout  octavo  volume  with  a  collection  of  the  more 
important  of  such  tables,  computed  for  different  coun- 
tries and  different  groups  of  the  population.  Now  they 
have  become  such  a  commonplace  that  elementary  classes 
in  vital  statistics  are  required  to  compute  them  (see  for 
example  Dublin's  New  Haven  life  table). 

CHANGES  IN  EXPECTATION  OF  LIFE 

I  wish  to  pass  in  graphic  review  some  of  these  life 
tables  in  order  to  call  attention  in  vivid  form  to  an  impor- 
tant fact  about  the  duration  of  human  life.  In  order  to 
bring  out  the  point  \vith  which  we  are  here  concerned  it 
will  be  necessary  to  make  use  of  another  function  of  the 
mortality  table  than  either  the  I  or  dx  lines  which  are 
shown  in  Figure  18.  I  msh  to  discuss  expectation  of 
life  at  each  age.  The  expectation  of  life  at  any  age  is 
defined  in  actuarial  science  as  the  mean  or  average  number 
of  years  of  survival  of  persons  alive  at  the  stated  age. 
It  is  got  by  dividing  the  total  survivor-years  of  after  life 
by  the  number  surviving  at  the  stated  age.  Or,  if  we  let 
e^  denote  what  is  called  the  curtate  expectation  of  life 

Ix  +  lx+l-'r  lx+2-^ -\-lx+n 

ex  = -J 

To  a  first  approximation,  sufficiently  accurate  for  our 
present  purposes,  the  total  expectation  of  life,  called  e^  , 
may  be  obtained  from  the  curtate  expectation  by  the 
simple  relation 

€l  =  ex  +  l/2 


THE  CHANCES  OF  DEATH 

TABLE  6 

Changes  in  expectation  oj  life  from  the  seventeenth  century  to 

the  present  time 


83 


Age 


0-  1 


2 
3 
4 
5 
6 
7 


1- 

2- 

3- 

4- 

5- 

6- 

7-  8 

8-  9 
9-10 

10-11 

11-12 

12-13 

13-14 

14-15 

15-16 

16-17 

17-18 

18-19 

19-20 

20-21 

21-22 

22-23 

23-24 

24-25 

25-26 

26-27 

27-28 

28-29 

29-30 

30-31 

31-32 

32-33 

33-34 

34-35 

35-36 

36-37 

37-38 

38-39 

39-40 

40-41 

41-42 

42-43 

43-44 

44-45 

45-46 

46-47 

47-48 

48-49 

49-50 


Average  length  of  life  remaining 

to  each   one  alive  at  beginning 

of  age  interval 


Breslau, 

17th 
century 


33.50 
38.10 
39.78 
40.75 
41.25 
41.55 
41.62 
41.16 
40.95 
40.50 
39.99 
39.43 
38.79 
38.16 
37.51 
36.86 
36.22 
35.57 
34.92 
34.26 
33.61 
32.95 
32.34 
31.67 
31.00 
30.38 
29.76 
29.14 
28.51 
27.93 
27.35 
26.76 
26 .  18 
25.59 
25.05 
24.51 
23.97 
23.43 
22.88 
22.33 
21.78 
21.23 
20.73 
20.23 
19.72 
19.22 
18.72 
18.21 
17.71 
17.25 


Carlisle, 

18th 
century 


38.72 

44.67 

47.55 

49.81 

50.76 

51.24 

51.16 

50.79 

50.24 

49.57 

48.82 

48.04 

47.27 

46.50 

45.74 

44.99 

44.27 

43.57 

42.87 

42.16 

41.46 

40.75 

40.03 

39.31 

38.58 

37.86 

37.13 

36.40 

35.68 

34.99 

34.34 

33.68 

33.02 

32.36 

31.68 

31.00 

30.32 

29.63 

2S .  95 

28.27 

27.61 

26.97 

26.33 

25.71 

25.08 

24.45 

23.81 

23.16 

22.. 50 

21.81 


U.S. 1910 


51.49 

57.11 

57.72 

57.44 

56.89 

56.21 

55.47 

54.69 

53.87 

53.02 

52.15 

51.26 

50.37 

49.49 

48.60 

47.73 

46,86 

46.01 

45.17 

44.34 

43.53 

42.73 

41.94 

41.16 

40.38 

39.60 

38.81 

38.03 

37.25 

36.48 

35.70 

34.93 

34.17 

33.41 

32.66 

31.90 

31.16 

30.42 

29.68 

28.94 

28.20 

27.46 

26.73 

25.99 

25.26 

24.54 

23.82 

23.10 

22.39 

21.69 


Age 


50-  51 

51-  52 

52-  53 

53-  54 

54-  55 
5.5-  56 

56-  57 

57-  58 

58-  59 

59-  60 

60-  61 

61-  62 

62-  63 

63-  64 

64-  65 

65-  66 

66-  67 

67-  68 

68-  69 

69-  70 

70-  71 

71-  72 

72-  73 

73-  74 

74-  75 

75-  76 

76-  77 

77-  78 

78-  79 

79-  80 

80-  81 

81-  82 

82-  83 

83-  84 

84-  85 

85-  86 

86-  87 

87-  88 

88-  89 

89-  90 

90-  91 

91-  92 

92-  93 

93-  94 

94-  95 

95-  96 

96-  97 

97-  98 

98-  99 
99-100 


Average  length  of  life  remaining 

to  each  one  alive  at  beginning 

of  age  interval 


Breslau, 

17th 
century 


16.81 

16.36 

15.92 

15.48 

14.99 

14.51 

14.02 

13.54 

13.06 

12.57 

12.09 

11.62 

11.14 

10.67 

10.20 

9.73 

9.27 

8.81 

8.36 

7.91 

7.53 

7.17 

6.85 

6.56 

6.25 

5.99 

5.79 

5.71 

5.66 

5.67 

5.74 

5.86 

6.02 

5.85 


Carlisle, 

l-Sth 
century 


21.11 

20.39 

19.68 

18.97 

18.27 

17.58 

16.89 

16.21 

15.55 

14.92 

14.34 

13.82 

13.31 

12.81 

12.30 

11.79 

11.27 

10.75 

10.23 


9 
9 


70 
17 
8.65 
8.16 
7.72 
7.33 
7.00 
6.69 
6.40 
6.11 
5.80 
5.51 
5.20 
4.93 
4.65 
4.39 
4.12 
3.90 
3.71 
3.59 
3.47 
3.28 
3.26 
3.37 


3. 

3. 

3 

3 

3 

3 

2 


48 
53 
53 
46 

28 
07 

,77 


U.S.1910 


20  98 
20.28 
19.58 
18.89 
18.21 
17.55 


16 
16 
15 
15 
14 
13 
13 
12 
12 
11 


90 
26 
64 
03 
42 
83 
26 
69 
14 
60 


11.08 
10,57 
10.07 
9,58 
9.11 
8.66 
8  22 
7.79 
7.38 
6,99 
6.61 
6.25 
5.90 
5.56 
5.25 
4.96 
4.70 
4.45 
4.22 
4.00 
3.79 
3.58 
3.39 
3.20 


.03 

.87 

.73 

.59 

.47 

.35 

2   24 

2   14 

2  04 

1.95 


In  each  of  the  series  of  diagrams  which  follow  there 
is  plotted  the  approximate  value  of  the  expectation  of 


84 


BIOLOGY  OF  DEATH 


life  for  some  group  of  people  at  some  period  in  the  more 
or  less  remote  past,  and  for  comparison  the  expectation 
of  life,  either  from  Glover's  table,  for  the  population  of 
the  United  States  Eegistration  Area  in  1910— the  expec- 
tation of  life  of  our  people  now,  in  short— or  equivalent 
figures  for  a  modern  English  or  French  population. 

Because  of  the  considerable  interest  of  the  matter, 
and  the  fact  that  the  data  are  not  easily  available  to 

HALLEY'5      BRLSLAU      1687-  1691     LIFL     TABLE. 


^ 


i 


10        Z?       "to       ti       30       35      40       45       i^       55       60       63       »        TS       30       dS       90      S      loO 

VLAPS    OF    Lire 
Pjg  19._Comparing  the  expectation  of  life  in  the  17th  century  with  that  of  the  present  time. 

biologists,  Table  6  is  inserted,  giving  the  expectations  of 
life  from  which  certain  of  the  diagrams  have  been  plotted. 
Figure  19  gives  the  results  from  Halley's  table,  based 
upon  the  mortality  experience  in  the  city  of  Breslau,  in 
Silesia,  during  the  years  1687  to  1691.  This  gives  us 
a  rough,  but  in  its  general  sweep  sufficiently  accurate 
picture  of  the  forces  of  mortality  towards  the  end  of  the 
seventeenth  century  From  this  diagram  it  appears  that 
at  birth  the  expectation  of  life  of  an  individual  born  in 
Breslau  in  the  seventeenth  century  was  much  lower  than 


THE  CHANCES  OF  DEATH  85 

that  of  an  individual  born  in  the  United  States  in  lUlO. 
The  difference  amounts  to  approximately  18  years! 
Probably  the  actual  difference  was  not  so  great  as  this, 
as  these  early  life  tables  are  kno\vn  to  be  inaccurate  at 
the  ends  of  the  lifespan,  particularly  at  the  beginning. 
At  10  years  of  age,  the  difference  in  expectation  of  life 
had  been  reduced  to  just  over  12  years;  at  age  20,  to  a 
little  less  than  10  years ;  at  age  30  to  7-%  years ;  at  age 
50  to  just  over  4  years;  at  age  70  to  I-V2  years.  At 
age  80  the  lines  have  crossed,  but  owing  to  the  inade- 
quate methods,  of  graduation  used  by  this  pioneer  actuary, 
together  with  the  paucity  and  probably  somewhat  inac- 
curate character  of  his  material,  no  stress  is  to  be  laid 
upon  the  crossing  of  the  lines,  or  upon  the  superior 
expectation  of  life  at  the  high  ages  in  the  seventeenth 
century  material.  What  the  diagram  shows  is  that  the 
expectation  of  life  at  early  ages  was  vastly  inferior 
in  the  seventeenth  century  to  what  it  is  now,  wliile  at 
advanced  ages  the  chances  of  living  were  substantially 
the  same.  Let  us  defer  the  further  discussion  of  the 
meaning  and  explanation  of  this  curious  fact  until  we 
have  examined  some  further  data. 

Figure  20  compares  the  expectation  of  life  in  England 
at  the  middle  of  the  eighteenth  century,  or  about  a  cen- 
tury later  than  the  last,  with  present  conditions  in  the 
United  States.  Again  we  see  that  the  expectation  at 
birth  was  greatly  inferior  then  to  what  it  is  now,  but  the 
difference  is  not  so  great  as  it  was  a  century  earlier, 
amounting  to  but  12-3/4  years  instead  of  the  18  we  found 
before.  Further  it  is  seen  that,  just  as  before,  the  expec- 
tations come  closer  together  with  advancing  age.  By 
the  time  age  45— middle  life— is  reached  the  expectation 
of  life  was  substantially  the  same  in  the  eighteenth  cen- 


86 


BIOLOGY  OF  DEATH 


tury  as  it  is  now.  At  age  47  the  eighteenth  century  line 
crosses  that  for  the  twentieth  century,  and  with  a  few 
trifling  exceptions,  notably  in  the  years  from  56  to  62, 
the  expectation  of  life  for  all  higher  ages  was  greater 
then  than  it  is  now.  We  see  in  the  eighteenth  century 
the  same  kind  of  result  as  was  indicated  in  the  seven- 
teenth, only  differing  in  degree. 


MILA'E'S      CARLISLE      UdO  -   1767     UFZ      TABLE 


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Fig.  20 — Comparing  the  expectation  of  life  in  the  18th  century  with  that  of  the  present  time. 

It  should  be  noted  that  all  data  as  to  mortality  in  the 
seventeenth  and  eighteenth  centuries  lack  the  degree  of 
accuracy  which  one  desires  for  purely  scientific  purposes. 
By  erring  generally  on  the  safe  side  these  old  mortality 
tables  did  well  enough  for  insurance  purposes.  But  quite 
different  results  as  to  the  detailed  values  of  life  table 
constants  in  these  early  periods  are  to  be  found  in  the 
literature.  For  example,  Richards  constructed  some 
life  tables  from  New  England  genealogical  records,  and 
compared  them  mth  Wiggles  worth's  table,  and  also  mth 
those  of  modern  times.     His  general  conclusion,  for  the 


THE  CHANCES  OF  DEATH  87 

New  England  population,  is:  'Hliat  during  tho  last  half- 
century  longevity*  in  Massachusetts,  and  probably  in 
New  England,  has  increased,  that  from  1793  to  1850  the 
increase  is  less  certain  and  from  the  seventeenth  to  the 
eighteenth  century  what  data  we  have  point  rather  to 
a  decrease  than  to  anything  else/^  This  result  may 
mean  any  one  of  a  number  of  things.  It  may  mean  merely 
inadequate  and  inaccurate  data  on  which  the  seventeenth 
century  tables  were  calculated.  It  may  mean  a  result  of 
less  stringent  selection  in  the  makeup  of  the  population 
with  the  passage  of  time.  In  any  case  it  applies  only  to 
a  small  and  rather  homogeneous  group  of  people. 

The  changes  in  expectation  of  life  from  the  middle 
of  the  seventeenth  century  to  the  present  time  where  the 
records  are  most  extensive  and  reliable  appear  to  fur- 
nish a  record  of  a  real  evolutionary  progression.  In  this 
respect  at  least  man  has  definitely  and  distinctively 
changed,  as  a  race,  in  a  period  of  three  and  a  half  cen- 
turies. This  is,  of  course,  a  matter  of  extraordinar\- 
interest,  and  at  once  stimulates  the  desire  to  go  still 
farther  back  in  history  and  see  what  the  expectation  of 
life  then  was.  Fortunately,  through  the  labors  of  Karl 
Pearson,  and  his  associate,  W.  K.  Macdonell,  it  is  pos- 
sible to  do  this,  if  not  with  precise  accuracy,  at  least 
to  a  rough  first  approximation.  Pearson  has  analyzed 
the  records  as  to  age  at  death  which  were  found 
upon  mummy  cases  studied  by  Professor  W.  Spiegelberg. 
These  mummies  belonged  to  a  period  between  1,900 
and  2,000  years  ago,  when  Egypt  was  under  Eoman 
dominion.  The  data  were  extremely  meagre,  but  from 
Pearson's   analysis    of   them   it    has    been    possible    to 

•  Richards  somewhat  loosely  uses  this  term  when  he  means  "expectation 
of  life." 


88 


BIOLOGY  OF  DEATH 


construct  the  diagram  which  is  shown  in  Figure  21. 
Each  circle  marks  a  point  where  it  was  possible  definitely 
to  calculate  an  expectation  of  life.  The  curve  running 
through  the  circles  is  a  rough  graphic  smoothing  of  the 
scattered  observed  data.  Unfortunately,  there  were  no 
records  of  deaths  in  early  infancy.     Either  there  were 


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Fig.  21. — Comparing  the  expectation  of  life  of  Ancient  Egyptians  with  that  of  present 
day  Americans.    Plotted  from  Pearson's  and  Glover's  data. 

For  comparison,  the  expectation  of  life  from  Glover's 
1910  United  States  life  table  is  inserted. 

It  will  be  seen  at  once  that  the  general  sweep  of  the 
line  is  of  the  same  sort  that  we  have  already  observed 
in  the  case  of  the  seventeenth  century  table.  In  the 
early  years  of  life  the  expectation  was  far  below  that  of 
the  present  time,  but  somewhere  between  ages  65  and  70 
the  Egyptian  line  crosses  the  modern  American  line,  and 
from  that  period  on  the  individuals  living  in  Egypt  at 
about  the  time  of  the  birth  of  Christ  could  apparently  look 
forward  to  a  longer  remaining  duration  of  life,  on  the  aver- 


THE  CHANCES  OF  DEATH  80 

age,  than  can  the  American  of  the  present  day.  Pearson's 
comment  on  this  fact  is  worth  quoting.  He  says:  ''In 
the  course  of  those  centuries  man  must  have  gro\vn  re- 
markably fitter  to  his  environment,  or  else  he  must  have 
fitted  his  environment  immeasurably  better  to  himself. 
No  civilized  community  of  to-day  could  show  such  a  curve 
as  the  civilized  Romano-Egyptians  of  2,000  years  ago 
exhibit.  We  have  here  either  a  strong  argument  for  the 
survival  of  the  physically  fitter  man  or  for  the  survival 
of  the  civilly  fitter  society.  Either  man  is  constitution- 
ally fitter  to  sur\dve  to-day,  or  he  is  mentally  fitter,  i.e., 
better  able  to  organize  his  civic  surroundings.  Both  con- 
clusions point  perfectly  definitely  to  an  evolutionary 
progress.  .  .  .  That  the  expectation  of  life  for  a 
Romano-Egyptian  over  68  was  greater  than  for  a  modern 
English  man  or  woman  is  what  we  might  expect,  for  ^\dth 
the  mortality  of  youth  and  of  middle  age  enormously 
emphasized  only  the  very  strongest  would  survive  to 
this  age.  Out  of  100  English  alive  at  10  years  of  age  39 
survive  to  be  68;  out  of  100  Romano-Egj^ptians  not  9 
survived.  Looking  at  these  two  curves  we  realize  at  a 
glance  either  the  great  physical  progress  of  man,  which 
enables  him  far  more  effectually  to  withstand  a  hostile 
environment,  or  the  great  social  and  sanitary  progress 
he  has  made  which  enables  him  to  modify  the  environ- 
ment. In  either  case  we  can  definitely  assert  that  2,000 
years  has  made  him  a  much  'fitter'  being.  In  this  com- 
parison it  must  be  remembered  that  we  are  not  placing 
a  civilized  race  against  a  barbaric  tribe,  but  comparing 
a  modern  civilization  with  one  of  the  liighest  types  of 
ancient  civilization. ' ' 

Macdonell  was  able  to  continue  this  investigation  on 
much  more  extensive  material  extracted  from  the  Corpus 


90 


BIOLOGY  OF  DEATH 


Inscriptionum  Latinarum  of  the  Berlin  Academy,  which 
gives  records  as  to  age  of  death  for  many  thousand 
Roman  citizens  dying,  for  the  most  part,  within  the  tirst 
three  or  four  centuries  of  the  Christian  era.  His  mate- 
rial may,  therefore,  be  taken  to  represent  the  conditions 
a  few  centuries  later  than  those  of  Pearson's  Romano- 
Egyptian  population.     Macdonell  was  able  to  calculate 


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YEARS   OF  AGC. 


Fig.    22. — Comparing  the  expectation  of  life  of  Ancient  Romans  with  that  of  present 
day  Americans.    Plotted  from  Macdonell's  and  Glover's  data. 

three  tables  of  expectation  of  life — the  first  for  Roman 
citizens  living  in  the  city  of  Rome  itself;  second  for 
those  living  in  the  provinces  of  Hispania  and  Lusitania ; 
and  tliird,  for  those  li\dng  in  Africa.  The  results  are 
plotted  against  the  United  States  1910  data,  as  before, 
in  Figures  22,  23,  and  24. 

Figure  22  relates  to  inhabitants  of  the  city  of  Rome 
itself.  The  deaths  from  wliich  the  expectations  are 
calculated  run  into  the  thousands,  and  fortunately  one 
is  able  to  separate  males  and  females.  As  in  Pearson's 
case,  which  we  have  just  examined,  modern  American 


THE  CHANCES  OF  DEATH 


91 


data  are  entered  for  comparison.  It  will  be  noted  at 
once  that  just  as  in  the  Ixomano-Egyptian  population  the 
expectation  of  life  of  inhabitants  of  ancient  Rome  was, 
in  the  early  years  of  life,  apparently  immensely  inferior  to 
that  of  the  modern  population.  From  about  the  age  of  60 
on,  however,  the  expectation  of  life  appears  to  have  been 
better  then  than  now.   Curiously  enough,  the  expectation 


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YEARS   or   A6L 

Fig.  23 — Comparing  the  expectation  of  life  of  the  population  of  the  Roman  provinces 
Hispania  and  Lusitania  with  that  of  present  day  Americans.     Plotted  from  Macdonell'B  and 

Glover's  data. 

of  life  of  females  was  poorer  at  practically  all  ages  of  life 
than  that  of  the  males  which  exactly  reverses  the  modern 
state  of  affairs.  Macdonell  believes  this  difference  to  be 
real  and  to  indicate  that  there  were  special  influences 
adversely  affecting  the  health  of  females  in  the  Roman 
Empire,  wliich  no  longer  operate  in  the  modern  world.  Up 
to  something  like  age  25  the  expectation  of  life  of  dwellers 
in  the  city  of  Rome  was  extremely  bad,  w^orse  than  in  the 
Romano-Eg}"ptian  population  which  Pearson  studied,  or 
in  the  populations  of  other  parts  of  the  Roman  Empire  as 
we  shall  see  in  the  following  diagram.     Macdonell  thinks 


92 


BIOLOGY  OF  DEATH 


that  this  difference  is  real  and  due  to  circumstances  pecu- 
liar to  Rome. 

The  general  features  of  the  diagram  for  the  popu- 
lation of  Hispania  and  Lusitania  (Figure  23)  are  similar 
to  those  that  we  have  seen,  with  the  difference  that  the 
expectation  of  life  up  to  age  20  or  25  is  not  as  bad  as  in 
the  city  of  Rome  itself.  Again  the  females  show  a  lower 
expectation  practically  throughout  life  than  do  the  males. 


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O        5        lO        15      20      25      30      35     40     45      60      65      60      65     70       16      60      C6      90      95     lOO 

YEARS    or   AGE 

FiQ.  24 — Comparing  the  expectation  of  life  of  the  population  of  the  Roman  provinces  in 
Africa  with  that  of  present  day  Americans.    Plotted  from  Macdonell's  and  Glover's  data. 

The  lines  cross  the  modern  American  lines  at  about  age 
60  and  from  that  point  on  these  colonial  Romans  appar- 
ently had  a  better  expectation  of  life  than  the  modern 
American  has. 

The  Romano-African  population  diagram  appears  to 
start  at  nearly  the  same  point  at  birth  as  does  the  modern 
American,  and  in  general  the  differences  up  to  age  35 
are  not  substantially  more  marked  from  modern  condi- 
tions than  they  are  in  the  seventeenth  century  Breslau 
table.     The  striking  thing,  however,  is  that  at  about  age 


THE  CHANCES  OF  DEATH  93 

40  the  lines  cross,  and  from  then  on  the  expectation  of 
life  was  definitely  superior  in  the  early  years  of  the 
Christian  era  to  what  it  is  now. 

It  should  be  said  that  the  curious  zigzagging  of  the 
Knes  in  all  of  these  Roman  tables  of  Macdonell  is  due  to 
the  tendency,  which  ancient  Romans  apparently  had  in 
common  with  present  day  American  negroes,  towards 
heavy  grouping  on  the  even  multiples  of  5  in  the  state- 
ment of  their  ages. 

Summarizing  the  whole  matter  we  see  that  during  a 
period  of  approximately  2,000  years  man's  expectation 
of  life  at  birth  and  subsequent  early  ages  has  apparently 
been  steadily  improving,  while  at  the  same  time  his  expec- 
tation of  life  at  advanced  ages  has  been  steadily  worsening. 
Thef  ormerphenomenon  may  probably  be  attributed  essen- 
tially to  ever  increasing  knowledge  of  how  best  to  cope 
with  the  lethal  forces  of  nature.*  Progressively  better 
sanitation,  in  the  broadest  sense,  do^\m  through  the  centur- 
ies has  saved  for  a  time  the  lives  of  ever  more  and  more 
babies  and  young  people  who  formerly  could  not  with- 
stand the  unfavorable  conditions  they  met,  and  died  in 
consequence  rather  promptly.  But  just  because  this  pro- 
cess tends  to  preserve  the  weaklings,  who  were  speedily 
eliminated  under  the  rigorous  action  of  unmitigated  nat- 

*  No  absolute  reliance  can,  of  course,  be  put  upon  Macdonell's  or 
Pearson's  curves.  Besides  laborintj  under  the  serious  actuarial  difficulty 
of  being  expectations  calculated  from  a  knowledge  of  deaths  alone,  the 
randomness  of  the  sampling,  even  on  that  basis,  is  extremely  doubtful. 
The  only  real  evidence  that  these  Roman  curves  represent  a  rough  pic- 
ture of  the  truth  as  to  expectation  of  life  in  those  days,  arises  from  the 
consideration  that  they  show  a  difference  from  present-day  expectations 
which  is  of  the  same  kind  as  that  which  is  found  between  populations  of 
one  and  two  centuries  ago  and  the  present,  and  of  a  greater  aiywunt,  as 
would  be  expected  from  the  longer  time  interval,  and  from  what  we  know 
has  occurred  in  the  material  development  of  civilization  in  the  meantime. 


94  BIOLOGY  OF  DEATH 

ural  selection,  there  appear  now  in  the  higher  age  groups 
of  the  population  many  weaker  individuals  than  formerly 
ever  got  there.  Consequently  the  average  expectation 
of  life  at  ages  beyond  say  60  to  70  is  not  nearly  so  good 
now  as  it  was  under  the  more  rigorous  regime  of  ancient 
times.  Then,  any  individual  who  attained  age  70  was 
the  surviving  resultant  of  a  bitterly  destructive  process 
of  selection.  To  run  successfully  the  gauntlet  of  early 
and  middle  life,  he  necessarily  had  to  have  an  extraor- 
dinarily vigorous  and  resistant  constitution.  Having 
come  through  successfully  to  70  years  of  age  it  is  no  mat- 
ter of  wonder  that  his  prospects  were  for  a  longer  old 
age  than  his  descendants  of  the  same  age  to-day  can  look 
forward  to.  Biologically,  these  expectation  of  life  curves 
give  us  the  first  introduction  to  a  principle  which  we 
shall  find  as  we  go  on  to  be  of  the  very  foremost  impor- 
tance in  fixing  the  span  of  human  longevity,  namely  that 
inherited  constitution  fund  anient  ally  and  primarily  de- 
termines how  long  an  individual  will  live, 

ANALYSIS  OF  THE  LIFE  TABLE 

I  shall  not  develop  tliis  point  further  now,  but  instead 
will  turn  back  to  consider  briefly  certain  features  of  the 
dx  line  of  a  life  table.  Figure  18  shows  that  this  line, 
which  gives  the  number  of  deaths  occurring  at  each  age, 
has  the  form  of  a  ver^^  much  stretched  letter  S  resting 
on  its  back.  Some  years  ago,  Pearson  undertook  the 
analysis  of  this  complex  curve,  and  drew  certain  inter- 
esting conclusions  as  to  the  fundamental  biological  causes 
lying  behind  its  curious  sinuosity.  His  results  are  shown 
in  Figure  25. 

He  regarded  the  dx  line  of  the  life  table  as  a  compound 
curve,  and  by  suitable  mathematical  analysis  broke  it  up 


THE  CHANCES  OF  DEATH 


95 


into  live  component  frequency  curves.  The  data  which  he 
used  were  furnished  by  the  d,  line  of  Ogle's  life  table, 
based  on  the  experience  of  1871  to  1880  in  England.  This 
line  gives  the  deaths  per  annum  of  one  thousand  persons 
born  in  the  same  year.  The  first  component  which  he  sepa- 
rated was  the  old  age  mortality.  This  is  shown  by  the 
dotted  curve  having  its  modal  point  between  70  and  75 
years,  at  the  point  lettered  Oi  on  the  base  of  the  diagram. 


PEARSON'S 

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Fio.  25. — Showing  Pearson's  results  in  fitting  the  dx  line  of  the  life  table  with  5  skew 
frequency  curves.    Plotted  from  the  data  of  Pearson's  original  memoir  on  "Skew  Variation" 

in  Phil.  Trans.  Roy.  Soc. 

This  com.ponent,  according  to  Pearson's  graduation, 
accounted  for  484.1  deaths  out  of  the  total  of  1,000,  or 
nearly  one-half  of  the  whole.  Its  range  extends  from 
under  20  years  of  age  to  the  upper  limit  of  life,  at  approx- 
imately 106  years.  The  second  component  includes  the 
deaths  of  middle  life.  This  is  the  smooth  curve  liaving 
its  modal  point  between  40  and  45  years  at  the  point  on 
the  base  marked  0..  Its  range  extends  from  about  5 
years  of  age  to  about  65.  It  accounts  for  175.2  deaths 
out  of  the  total  of  1,000.     It  is  a  long,  much  spread  out 


96  BIOLOGY  OF  DEATH 

curve,  exhibiting  great  variability.  The  third  compo- 
nent is  made  up  by  the  deaths  of  youth.  This  accounts 
for  50.8  deaths  out  of  the  total  of  a  thousand,  and  its 
range  extends  from  about  the  time  of  birth  to  nearly  45 
yea^rs.  Its  mid-point  is  between  20  and  25  years,  and  it 
exhibits  less  variability  than  either  the  middle  life  or  the 
old  age  curves.  The  fourth  component,  the  modal  point 
of  which  is  at  the  point  on  the  base  of  the  diagram  marked 
O4  covers  the  childhood  mortality.  It  accounts  for  46-4 
deaths  out  of  the  total  of  1,000.  Its  range  and  variability 
are  ob\dously  less  than  those  of  any  of  the  other  three 
components  so  far  considered.  The  last,  excessively  skew 
component,  is  that  which  describes  the  mortality  of  in- 
fancy. It  is  given  by  a  J  shaped  curve  accounting  for 
245.7  deaths  after  birth,  and  an  antenatal  mortality  of 
605.  In  order  to  get  any  fit  at  all  for  this  portion  of  the 
mortality  curve  it  is  necessary  to  assume  that  the  deaths 
in  utero  and  those  of  the  first  months  after  birth  are  a 
homogeneous  connected  group. 

Summing  all  these  components  together  it  is  seen 
that  the  resulting  smooth  curve  very  closely  fits  the  series 
of  small  circles  which  are  the  original  observations. 
From  the  standpoint  merely  of  curve  fitting  no  better 
result  than  this  could  be  hoped  for.  But  about  its  bio- 
logical significance  the  case  is  not  quite  so  clear,  as  we 
shall  presently  see. 

Pearson  himself  thinks  of  these  five  components  of 
the  mortality  curve  as  typifying  five  Deaths,  shooting 
with  different  weapons,  at  different  speeds  and  with  dif- 
fering degrees  of  precision  at  the  procession  of  human 
beings  crossing  the  Bridge  of  Life.  The  first  Death  is, 
according  to  Pearson,  a  marksman  of  deadly  aim,  con- 
centrated fire,  and  unremitting  destructiveness.     He  kills 


THE  CHANCES  OF  DEATH  97 

before  birth  as  well  as  after  and  may  be  conceived  as 
beating  down  young  lives  with  the  bones  of  their  ances- 
tors. The  second  marksman  who  aims  at  childhood  has 
an  extremely  concentrated  fire,  which  may  be  typified 
by  the  machine  gun.  Only  because  of  the  concentration 
of  tliis  fire  are  we  able  to  pass  through  it  witliout  appal- 
ling loss.  The  third  marksman  Death,  who  shoots  at 
youth  has  not  a  very  deadly  or  accurate  weapon,  perhaps 
a  bow  and  arrow.  The  fire  of  the  fourth  marksman  is 
slow,  scattered  and  not  very  destructive,  such  as  might 
result  from,  an  old  fashioned  blunderbuss.  The  last  Death 
plies  a  rifle.  None  escapes  his  shots.  He  aims  at  old  age 
but  sometimes  hits  youth.  His  unremitting  activity 
makes  his  toll  large. 

We  may  let  Pearson  sum  the  whole  matter  up  in  his 
own  words :  *  ^  Our  investigations  on  the  mortality  statis- 
tics have  thus  led  us  to  some  very  definite  conclusions 
with  regard  to  the  chances  of  death.  Instead  of  seven 
we  have  five  ages  of  man,  corresponding  to  the  periods 
of  infancy,  of  childhood,  of  youth,  of  maturity  or  middle 
age,  and  of  senility  or  old  age.  In  the  case  of  each  of 
these  periods  we  see  a  perfectly  regular  chance  distri- 
bution, centering  at  a  given  age,  and  tailing  off  on  either 
side  according  to  a  perfectly  clear  mathematical  law.  .  . 

**  Artistically,  we  no  longer  thinlv  of  Death  as  striking 
chaotically;  we  regard  his  aim  as  perfectly  regular  in 
the  mass,  if  unpredictable  in  the  individual  instance.  It 
is  no  longer  the  Dance  of  Death  wliich  pictures  for  us 
Death  carrying  off  indiscriminately  the  okl  and  young, 
the  rich  and  the  poor,  the  toiler  and  the  idler,  the  babe 
and  its  grandsire.  We  see  something  quite  different, 
the  cohort  of  a  thousand  tiny  mites  starting  across  the 
Bridge  of  Life,  and  growing  in  stature  as  they  advance, 

7 


98  BIOLOGY  OF  DEATH 

till  at  the  far  end  of  the  bridge  we  see  only  the  gray- 
beard  and  the  4ean  and  slippered  pantaloon.'  As  they 
pass  along  the  causeway  the  throng  is  more  and  more 
thinned ;  five  Deaths  are  posted  at  different  stages  of  the 
route  longside  the  bridge,  and  with  different  skewness 
of  aim  and  different  weapons  of  precision  they  fire  at 
the  human  target  till  none  remains  to  reach  the  end  of  the 
causeway — the  limit  of  life/' 

This  whole,  somewhat  fanciful,  conception  of  Pear- 
son's needs  a  little  critical  examination.  What  actually 
he  has  done  is  to  get  a  good  empirical  fit  of  the  dx  line 
by  the  use  of  equations  involving  all  told  some  17  con- 
stants. Because  the  combined  curve  fits  well,  and  funda- 
mentally for  no  other  reason,  he  implicitly  concludes 
that  the  fact  that  the  fit  is  got  by  the  use  of  five  compo- 
nents means  biologically  that  the  dx  line  is  a  compound 
curve,  and  indicates  a  five-fold  biological  heterogeneity  in 
the  material.  But  it  is  a  very  hazardous  proceeding  to 
draw  biological  conclusions  of  this  type  from  the  mere 
fact  that  a  theoretical  mathematical  function  or  functions 
fits  well  a  series  of  observational  data.  I  fully  discussed 
this  point  several  years  ago  and  pointed  out: 

**The  kind  of  evidence  under  discussion  can  at  best 
have  but  inferential  significance;  it  can  never  be  of  de- 
monstrative worth.  It  is  based  on  a  process  of  reasoning 
which  assumes  a  fundamental  or  necessary  relationship 
to  exist  between  two  sets  of  phenomena  because  the  same 
curve  describes  the  quantitative  relations  of  both  sets. 
A  little  consideration  indicates  that  tliis  method  of  rea- 
soning certainly  cannot  be  of  general  application,  even 
though  we  assume  it  to  be  correct  in  particular  cases. 
The  difficulty  arises  from  the  fact  that  the  mathematical 
functions  commonly  used  with  adequate  results  in  physi- 


THE  CHANCES  OF  DEATH  99 

cal,  chemical,  biological,  and  mathematical  investigations 
are  comparatively  few  in  number.  The  literature  of 
science  shows  nothing  clearer  than  that  the  same  type 
of  curve  frequently  serves  to  describe  witli  complete 
accuracy  the  quantitative  relations  of  widely  different 
natural  phenomena.  As  a  consequence,  any  proposition 
to  conclude  that  two  sets  of  phenomena  are  causally  or 
in  any  other  way  fundamentally  related  solely  because 
they  are  described  by  the  same  type  of  curve  is  of  a  very 
doubtful  validity. '' 

Henderson  has  put  Pearson's  five  components  together 
in  a  single  equation,  as  follows  : 

7.7525 

(3._715\    '  0.2215  (a;— 71.5)  — [.05524  (x— 41.5)  p 

1 35^~  )  ^  +5.4e 

—  [.09092  (x  —  22.5)P 
+  2.6  e  -f  8.5  (x  —  2^  "^^ ''^  ^  —  .3271  (x  —  3) 

+  415.6(.  +  .75)-^^-7^^-  +  -7^) 

Henderson  says  regarding  this  method  of  Pearson  \s 
for  analyzing  the  life  table:  ^^  .  .  it  is  difficult  to  lay  a 
firm  foundation  for  it,  because  no  analysis  of  the  deaths 
into  natural  divisions  by  causes  or  otherivise  has  yet  been 
made  such  that  the  totals  in  the  various  groups  would 
conform  to  those  frequency  curv^es."  The  italics  in  this 
quotation  are  the  present  writer's  for  the  purpose  of  em- 
phasizing the  crucial  point  of  the  whole  matter. 

Now  it  is  altogether  probable  that  one  could  get  just 
as  good  a  fit  to  the  observed  dr  line  as  is  obtained  by 
Pearson's  five  components  by  using  a  17  constant  equa- 
tion of  the  type 

y  z=  a -\- bx -{- cx^ -\- dx* -{- ex*  +  fx^  +  gx' + -i-  rtj" 


100  BIOLOGY  OF  DEATH 

and  in  that  event  one  wonld  be  quite  as  fully  justified 
(or  really  unjustified)  in  concluding  that  the  dx  line  was 
a  homogeneous  curve  as  Pearson  is  in  concluding  from 
his  five-component  fit  that  it  is  compound.  Indeed  Witt- 
stein's  formula  involving  but  four  constants 

n  n 

—  (M  —  x)  J      —  (mx) 

qx  =  a  +  ~  ^ 

m 

gives  a  substantially  good  fit  over  the  whole  range  of  life. 
It  is,  of  course,  apparent  that  the  formula  as  here  given 
is  in  terms  of  another  function,  q^ ,  of  the  life  table,  rather 
than  the  dx  which  we  have  hitherto  been  discussing.  But 
no  difference  is  in  fact  involved,  q^  values  may  be  imme- 
diately converted  into  dx  values  by  a  simple  arithmeti- 
cal transformation. 

But  in  neither  Pearson's,  Wittstein's,  nor  any  other 
case  is  the  curve-fitting  evidence,  by  and  of  itself,  in  any 
sense  a  demonstration  of  the  biological  homogeneity  or 
heterogeneity  of  the  material.  Of  far  greater  impor- 
tance, and  indeed  conclusive  significance,  is  the  fact,  to 
be  brought  out  in  a  later  chapter,  that  in  material  experi- 
mentally known  to  he  biologically  homogeneous ^  a  popu- 
lation made  up  of  full  brothers  and  sisters  out  of  a  brother 
X  sister  mating  and  kept  throughout  life  in  a  uniform 
enviroimient  identical  for  all  individuals,  one  gets  a  dx 
line  in  all  its  essential  features,  save  for  the  absence  of 
excessive  infant  mortality  arising  from  perfectly  clear 
biological  causes,  identical  with  the  human  dx  line.  It 
has  long  been  apparent  to  the  thoughtful  biologist  that 
there  was  not  the  slightest  biological  reason  to  suppose 
that  the  peculiar  sinuosity  of  the  human  dx  line  owed  its 
origin  to  any  fundamental  heterogeneity  in  the  material, 
or  differentiation  in  respect  of  the  forces  of  mortality. 


THE  CHANCES  OF  DEATH  101 

Now  we  have  experimental  proof,  to  be  discussed  in  a 
later  chapter,  that  with  complete  homogeneity  of  the 
material,  both  genetic  and  environmental,  one  gets  just 
the  same  kind  of  d^  line  as  in  normal  human  material. 
We  must  then,  I  think,  come  to  the  conclusion  that  bril- 
liant and  picturesque  as  is  Pearson's  conception  of  the 
^ve  Deaths,  actually  there  is  no  slightest  reason  to  sup- 
pose that  it  represents  any  biological  reality,  save  in  the 
one  respect  that  his  curve  fitting  demonstrates,  as  any 
other  equally  successful  would,  that  deaths  do  not  occur 
chaotically  in  respect  of  age,  but  instead  in  a  regular 
manner  capable  of  representation  by  a  mathematical 
function  of  age. 

An  interesting  and  suggestive  analysis  of  the  4  line, 
resting  upon  a  sounder  biological  basis  than  Pearson's, 
has  lately  been  given  by  Arne  Fisher.  He  breaks  the 
curve  up  into  8  or  9  components,  based  upon  the  compar- 
atively stable  values  of  the  death  ratios  for  different 
groups  of  diseases  characteristic  of  different  ages.  The 
resulting  total  curve  fits  the  facts  from  age  10  on,  very 
well,  and  makes  possible  the  calculation  of  a  complete 
life  table  from  a  knowledge  of  deaths  only. 


CHAPTER  IV 

i 

THE  CAUSES  OF  DEATH 

It  has  been  suggested  in  earlier  chapters  that  natural 
death  of  the  metazoan  body  may  come  about  fundamen- 
tally because  of  the  differentiation  and  consequent  mu- 
tual dependence  of  structure  and  function  of  that 
body.  It  is  a  complex  aggregate  of  cells  and  tissues, 
all  mutually  dependent  upon  each  other  and  in  a 
delicate  state  of  adjustment  and  balance.  If  one  organ 
for  any  accidental  reason,  whether  internal  or  external, 
fails  to  function  normally  it  upsets  this  delicate  balance, 
and  if  normal  functioning  of  the  part  is  not  promptly 
restored,  death  of  the  whole  organism  eventually  results. 
Furthermore,  it  is  apparent  that  death  does  not  strike  in 
a  haphazard  or  random  manner,  but  instead  in  a  most 
orderly  way.  There  are  certain  periods  of  life — notably 
youth — where  only  an  insignificant  fraction  of  those  ex- 
posed to  risk  ever  die.  At  other  ages,  as,  for  example, 
extreme  old  age  and  early  infancy,  death  strikes  with 
appalling  precision  and  frequency.  Further  we  recall 
with  Seneca  that  fiascimus  uno  modo  ynultis  morimur. 
Truly  there  are  many  ways  of  dying.  The  fact  is  obvious 
enough.  But  what  is  the  biological  meaning  of  this  mul- 
tiplicity of  pathways  to  the  river  Styx?  There  is  but 
one  pathway  into  the  world.  Why  so  many  to  go  out? 
To  the  consideration  of  some  phases  of  this  problem 
attention  is  directed  in  this  chapter. 

By  international  agreement  among  statisticians  the 
causes  of  human  mortality  are,  for  statistical  purposes, 

102 


THE  CAUSES  OF  DEATH  103 

rather  rigidly  defined  and  separated  into  somethin.ir  over 
180  distinct  units.  It  should  be  clearly  understood  that 
this  convention  is  distinctly  and  essentially  statistical  in 
its  nature.  In  recording  the  statistics  of  death  the  regis- 
trar is  confronted  wdth  the  absolute  necessity  of  putting 
every  demise  into  some  category  or  other  in  respect  of 
its  causation.  However  complex  biologically  may  have 
been  the  train  of  events  leading  up  to  a  particular  end, 
the  statistician  must  record  the  terminal  *' cause  of  death'* 
as  some  particular  thing.  The  International  Classifica- 
tion of  the  Causes  of  Death  is  a  code  which  is  the  result 
of  many  years'  experience  and  thought.  Great  as  are 
its  defects  in  certain  particulars,  it  nevertheless  has  cer- 
tain marked  advantages,  the  most  conspicuous  of  which 
is  that  by  its  use  the  vital  statistics  of  different  countries 
of  the  world  are  put  upon  a  uniform  basis. 

The  several  separate  causes  of  death  are  grouped  in 
the  International  Classification  into  fourteen  general 
classes.     These  are: 

I.  General  diseases. 

II.  Diseases  of  the  nervous  system  and  of  the  organs  of  special  sense. 

III.  Diseases  of  the  circulatory  system. 

IV.  Diseases  of  the  respiratory  system. 
V.  Diseases   of   the   digestive    system. 

VI.  Non-venereal  diseases  of  the  genito-urinary  system  and  annexa. 

VII.  The  puerperal  state. 

VIII.  Diseases  of  the  skin  and  of  the  cellular  ti.isue. 

IX.  Diseases  of  the  bones  and  organs  of  locomotion. 

X.  Malformation. 

XI.  Early   infancy. 

XII.  Old  age. 

XIII.  External  causes. 

XIV.  Ill-defined  diseases. 

Perhaps  the  most  outstanding  feature  which  strikes 
one  about  the  International  List  is  that  it  is  not  primarily 


104  BIOLOGY  OF  DEATH 

a  biological  classification.  Its  first  group,  for  example, 
called  ^^ General  Diseases,"  wMch  caused  in  1916  in  the 
Registration  Area  of  the  United  States  approximately 
one-fourth  of  all  the  deaths,  is  a  most  curious  biological 
and  clinical  melange.  It  includes  such  diverse  entities  as 
measles  and  malaria,  tetanus  and  tuberculosis,  cancer 
and  gonococcus  infection,  alcoholism  and  goiter,  and 
many  other  unlike  causes  of  death.  For  the  purposes  of 
the  statistical  registrar  it  perhaps  has  useful  points  to 
make  this  ^^ General  Diseases"  grouping,  but  it  clearly 
corresponds  to  nothing  natural  in  the  biological  world. 
Again  in  such  parts  of  the  scheme  as  do  have  some 
biological  foundation  the  basis  is  different  in  different 
rubrics.  Some  have  an  organological  basis,  while  others 
have  a  causational. 

For  purposes  of  biological  analysis,  I  developed  some 
time  ago  an  entirely  different  classification  of  the  causes 
of  death,  on  what  appears  to  be  a  reasonably  consistent 
basis.*  The  underlying  idea  of  this  new  classification 
was  to  group  all  causes  of  death  under  the  heads  of  the 
several  organ  systems  of  the  body,  the  functional  break- 
down of  which  is  the  immediate  or  predominant  cause  of 
the  cessation  of  life.  All  except  a  few  of  the  statistically 
recognized  causes  of  death  in  the  International  Classifi- 
cation can  be   assigned  places   in   such   a  biologically 

*  It  should  be  clearly  understood  that  I  am  not  advocating  a  new 
classification  of  the  causes  of  death  for  statistical  use.  I  should  oppose 
vigorously  any  attempt  to  substitute  a  new  classification  (mine  or  any 
other)  for  the  International  List  now  in  use.  Uniformity  in  statistical 
classification  is  essential  to  usable,  practical  vital  statistics.  Such  uni- 
formity has  now  become  well  established  through  the  International  Classi- 
fication. It  would  be  most  undesirable  to  make  any  radical  changes  in  the 
Classification  now,  I  have  made  a  rearrangement  of  the  causes  of  death,  for 
the  purposes  of  a  specific  biological  problem,  and  no  other.  I  am  not 
"proposing  a  new  classification  of  vital  statistics"  for  official  or  any  other 
use  except  the  one  to  which  it  is  here  put. 


THE  CAUSES  OF  DEATH  105 

grouped  list.  It  has  a  sound  logical  foundation  in  the 
fact  that,  biologically  considered,  death  results  because 
some  organ  system,  or  group  of  organ  systems,  fails  to 
continue  its  functions. 

The  headings  finally  decided  upon  in  the  new  classi- 
fication were  as  follows: 

I.  Circulatory  system,  blood  and  blood-forming  organs, 

II.  Respiratory  system. 

III.  Primary  and  secondary  sex  organs. 

IV.  Kidneys  and  related  excretory  organs. 
V.  Skeletal  and  muscular  systems. 

VI.  Alimentary  tract  and  associated  organs  concerned  in  metabolism. 

VII.  Nervous  system  and  sense  organs. 

VIII.  Skin. 

IX.  Endocrinal  system. 

X.  All   other  causes   of   death. 

The  underlying  idea  of  this  rearrangement  of  the 
causes  of  death  is  to  put  all  those  lethal  entities  together 
which  bring  about  death  because  of  the  functional  organic 
breakdown  of  the  same  general  organ  system.  The  cause 
of  this  functional  breakdo^^^l  may  be  anything  w^hatever 
in  the  range  of  pathology.  It  may  be  due  to  bacterial 
infection;  it  may  be  due  to  trophic  disturbances;  it  may 
be  due  to(  mechanical  disturbances  which  prevent  the 
continuation  of  normal  function;  or  to  any  cause  what- 
soever. In  other  words  the  basis  of  the  classification  is 
not  that  of  pathological  causation,  but  it  is  rather  that 
of  organological  breakdowai.  We  are  now  looking  at 
the  question  of  death  from  the  standpoint  of  the  biologist, 
who  concerns  himself  not  with  what  causes  a  cessation  of 
function,  but  rather  mth  what  part  of  the  organism  ceases 
to  function,  and  therefore  causes  death. 

In  a  series  of  papers  already  published  I  have  given 
a  detailed  account  of  this  classification,  and  the  reasoning 
on  which  particular  causes  of  death  are  placed  in  it  where 


106  BIOLOGY  OF  DEATH 

they  are.  Space  is  lacking  here  to  go  into  the  details, 
and  I  must  consequently  ask  the  reader  either  to  take  it 
on  faith  for  the  time  being  that  the  classification  is  at 
least  a  fairly  reasonable  one,  or  to  take  the  trouble  to 
go  over  it  in  detail  in  the  original  publication.* 

GENERAL  RESULTS   OF  BIOLOGICALLY  CLASSIFIED  DEATH  RATES 

Here  I  should  like  to  present  first  some  general  statis- 
tical results  of  this  classification.  The  data  which  we 
shall  first  discuss  are  in  the  form  of  death  rates,  from 
various  causes,  per  hundred  thousand  living  at  all 
ages,  arranged  by  organ  systems  primarily  concerned 
in  death  from  specified  diseases.  The  statistics  came 
from  three  widely  separated  localities  and  times,  viz., 

(a)  from  the  Registration  Area  of  the  United  States; 

(b)  from  England  and  Wales;  and  (c)  from  the  City  of 
Sao  Paulo,  Brazil. 

The  summarized  results  are  shown  in  Table  7,  and  in 
graphic  form  in  Figure   26. 

The  rates  are  arranged  in  descending  order  of  magni- 
tude for  the  United  States  Registration  Area,  with  the 
exception  of  those  of  group  X,  all  other  causes  of  death. 
We  note  in  passing  that  this  biologically  unclassifiable 
group  includes  roughly  10  to  15  per  cent  of  the  total 
mortality.  It  may  be  well  to  digress  a  moment  to  con- 
sider why  these  deaths  cannot  be  put  into  our  general 
scheme.     Table  8  exhibits  the  rates  included  in  class  X. 

This  residue  comprises  in  general  three  categories 
(a)   accidental  and  homicidal  deaths;   (h)   senility;  and 

*  Cf.  particularly  Pearl,  R,  "  On  the  embryological  basis  of  human 
mortality."  (Proc.  Natl.  Acad.  Sci.  Vol.  5,  pp.  593-598,  1919)  and  "Cer- 
tain evolutionary  aspects  of  human  mortality  rates."  (Amer.  Natl.  Vol. 
LIV.  pp.  5-44,  1920).  The  following  section  as  well  as  Chapter  V  are 
largely  based  upon  the  second  of  the  two  papers. 


THE  CAUSES  OF  DEATH  107 

(c)  deaths  from  a  variety  of  causes  wliieh  are  statisti- 
cally lumped  together  and  camiot  be  disentangled.  Ac- 
cidental and  homicidal  deaths  find  no  place  in  a  biologi- 

TABLE  7 

Showing  the  Relative  Importance  of  Different  Organ  Systems  in 

Human  Mortality 


Group 
No. 


II 
VI 

I 

VII 

IV 

III 

V 

VIII 

IX 


X 


Orean  System 


Respiratory  system 

Alimentary  tract  and  associated 

organs  

Circulatory  system,  blood 

Nervous  system  and  sense  organs  . 
Kidneys    and    related    excretory 

organs  

Primary  and  secondary  sex  organs, 
Skeletal  and  muscular  system  .  . . 

Skin 

Endocrinal  system 


Total  death  rate  classifiable  on  a 
biological  basis 


All  other  causes  of  death 


Death  Rates  per  100.000 


Registration  Area, 
U.  S.  A. 


1906-10 


395.7 

334.9 
209.8 
175.6 

107.2 

88.1 

12.6 

10.1 

1.5 


1,335.5 


171.3 


1901-05 


460.5 

340.4 
190.8 
192.9 

107.4 

77.4 

13.7 

13.3 

1.2 


1,403.6 


211.8 


England 

and 

Wales 

1914 


420.2 

274.1 
208.6 
151.9 

19.4 
95.4 
18.2 
12.0 
1.9 


Sao 

Paulo 
1917 


1,201.7 


141.4 


417.5 


613.8 
254.8 
124.3 

83.4 

103.2 

6.8 

7.9 

1.1 


1,612.8 


109.8 


cal  classification  of  mortality.  A  man  organically  sound 
in  every  respect  may  be  instantly  killed  by  being  struck 
by  a  railroad  train  or  an  automobile.  The  best  possible 
case  that  could  be  made  out  for  a  biological  factor  in  such 
deaths  would  be  that  contributory  carelessness  or  negli- 
gence, which  is  a  factor  in  some  portion  of  accidental 
deaths,  bespeaks  a  small  but  definite  organic  mental  in- 
feriority or  weakness,  and  that,  therefore,  accidental 
deaths  should  be  charged  against  the  nervous  system. 
This,  however,  is  obviously  not  sound.  Yov,  in  the  lirst 
place,  in  many  accidents  there  is  no  factor  of  contributory 


SYSTEM 


AUM5NTARV 
T/?ACT  AND 
ASSOCIATED 
ORGANS 


CIRCULATORY 

SYSTEM. 

BLOOD 


NERVOUS 
SYSTEM  /JW 
SENSE 
ORGANS 


KIDNEYS  AND 
RELATED 
EXCRETORY 
ORGANS 


PRIMARY  AND 
SECONDARY 
SEX  ORGANS 


M^MpMM^^#^^ 

[ji ffi„i.ii....iJ.iEi i..i.i,„.i 

335.7 

4ao.a 

417.5 


SKELETAL  AND\ 

MUSCULAR 

SYSTEfYI 


SKIN 


ENDCCRINAL 
SYSTEM 


m  613.3 


mra 


US-  REG  AREA    1306-10       ENGLAND  a^o  WALES  f9l4    SAO  PAULO   1911 
FiQ.  26. — Showing  the  relative  importance  of  the  different  organ  systems  in  human  mortahty. 


THE  CAUSES  OF  DEATH 


109 


negligence  in  fact,  and,  in  the  second  place,  in  those  cases 
where  such  negligence  can  fairly  be  alleged  its  degree  or 
significance  is  undeterminable  and  in  many  cases  surely 
slight. 

Senility  as  a  cause  of  death  is  not  further  classifiable 

TABLE  8 
All  Other  Causes 


No. 


187, 

188  & 

189 

154 

45 

152* 

34 

46 

55 

153 

19 


"  Cause  of  Death  "  as  per  International 
Classification 


All  external  causes  (except  suicide) 


Ill-defined  diseases 

Senility 

Cancer  of  other  organs  or  of  organs 
not  specified 

Other  causes  peculiar  to  early  in- 
fancy   

Tuberculosis  of  other  organs 

Other  tumors  (female  genital  or- 
gans excepted) 

Other  general  diseases 

Lack  of  care 

Other  epidemic  diseases 


Totals 


Registration  Area, 
U.  S.  A. 

England 

and 

Wales 

1914 

11906-10 

1901-05 

91.9 

87.8 

26.1 

29.4 

47.8 

7.3 

29.0 

41.0 

81.5 

12.9 

16.1 

16.6 

3.4 

2.6 

5.1 

2.1 

2.0 

1.6 

1.0 

1.5 

0.5 

1.0 

0.5 

1.5 

0.3 

12.3 

0.6 

0.3 

0.2 

0.6 

171.3 

211.8 

141.4 

Sfto 

Paulo 

1917 


36.4 


36.3 
11.1 

17.9 

3.3 
0.2 

0.9 
3.5 
0 
0.2 

109.8 


*  In  part. 

on  an  organological  basis.  A  death  really  due  to  old 
age,  in  the  sense  of  Metchnikoff,  represents,  from  the 
point  of  view  of  the  present  discussion,  a  breaking  down 
or  wearing  out  of  all  the  organ  systems  of  the  body  con- 
temporaneously. In  a  strict  sense  tliis  probably  never, 
or  at  best  extremely  rarely,  happens.  But  physicians 
and  registrars  of  mortality  still  return  a  certain  number 
of  deaths  as  due  to  ^^senilitv.''     Under  the  circumstances 


no  BIOLOGY  OF  DEATH 

it  is  not  possible  to  go  behind  such  returns  biologically. 

The  second  line  of  Table  8,  ''Ill-defined  diseases," 
furnishes  a  striking  commentary  on  the  relative  efficiency 
of  the  medical  profession  in  the  United  States  and  Eng- 
land in  respect  of  the  reporting  of  the  causes  of  death. 
Only  about  one-fourth  as  many  deaths  appear  in  the 
English  vital  statistics  as  due  to  ill-defined  and  unlalo^vn 
causes  as  in  the  United  States  figures. 

Returning  now  to  the  consideration  of  the  general 
results  set  forth  in  Table  7  and  Figure  26,  a  number  of 
interesting  points  about  human  mortality  are  apparent. 
In  the  United  States,  during  the  decade  covered,  more 
deaths  resulted  from  the  breakdown  of  the  respiratory 
system  than  from  the  failure  of  any  other  organ  system 
of  the  body.  The  same  thing  is  true  of  England  and 
Wales.  In  Sao  Paulo  the  alimentary  tract  takes  first 
position,  with  the  respiratory  system  a  rather  close 
second.  The  tremendous  death  rate  in  Sao  Paulo  charge- 
able to  the  alimentary  tract  is  chiefly  due  to  the  relatively 
enormous  number  of  deaths  of  infants  under  two  from 
diarrhoea  and  enteritis.  Nothing  approaching  such  a 
rate  for  this  category  as  Sao  Paulo  shows  is  known  in 
this  country  or  England. 

In  all  three  localities  studied  the  respiratory  and  the 
alimentary  tract  together  account  for  rather  more  than 
half  of  all  the  deaths  biologically  classifiable.  These  are 
the  two  organ  systems  which,  while  physically  internal, 
come  in  contact  directly  at  their  surfaces  with  environ- 
mental entities  (water,  food,  air)  mth  all  their  bacterial 
contamination.  The  only  other  organ  system  directly 
exposed  to  the  environment  is  the  skin.  The  alimentary 
canal  and  the  lungs  are,  of  course,  in  effect  invaginated 
surfaces  of  the  body.  The  mucous  membranes  which 
line  them  are  far  less  resistant  to  environmental  stresses, 


THE  CAUSES  OF  DEATH  111 

both  physical  and  chemical,  than  is  the  skin  with  its  pro- 
tecting layers  of  stratified  and  cornified  epithelium. 

The  organs  concerned  with  the  blood  and  its  circula- 
tion— the  heart,  arteries  and  veins,  etc. — stand  third  in 
importance  in  the  mortality  list.  Biologically  the  blood, 
through  its  immunological  mechanism,  constitutes  the 
second  line  of  defense  which  the  body  has  against  noxious 
invaders.  The  first  line  is  the  resistance  of  the  outer 
cells  of  the  skin  and  the  lining  epithelium  of  alimentary 
tract,  lungs,  and  sexual  and  excretory  organs.  When 
invading  organisms  pass  or  break  down  these  first  two 
lines  of  defense,  the  battle' is  then  with  the  home  guard,  the 
cells  of  the  organ  system  itself,  which,  like  the  industrial 
workers  of  a  commonwealth,  keep  the  body  going  as  a 
whole  functioning  mechanism.  Naturally  it  would  1)e  ex- 
pected that  the  casualties  would  be  far  heavier  in  the  first 
two  defense  lines  (respiratory  and  alimentary  systems 
and  the  blood  and  circulation)  than  in  the  home  guard. 
Death  rates,  when  biologically  classified,  bear  out  this 
expectation. 

In  the  United  States  the  kidneys  and  related  excre- 
tory organs  are  responsible  for  more  deaths  than  the  sex 
organs.  This  relation  is  reversed  in  England  and  Wales, 
and  in  Sao  Paulo.  This  difference  is  mainly  due  in  both 
countries  to  premature  birth.  The  higher  premature 
birth  rate  for  these  two  localities  as  compared  with  the 
United  States  might  conceivably  be  explained  in  any  one 
of  several  ways.  It  might  mean  better  obstetrics  here 
than  in  the  other  localities,  or  it  might  mean  that  the 
women  of  this  country,  as  a  class,  are  somewhat  superior 
physiologically  in  the  matter  of  reproduction,  when  they 
do  reproduce,  or  it  might  be  in  some  manner  connected 
with  differences  in  birth  rates. 


112  BIOLOGY  OF  DEATH 

The  last  three  organ  systems,  skeletal  and  muscular 
system,  skin  and  endocrinal  organs,  are  responsible  for 
so  few  deaths  relatively  as  not  to  be  of  serious  moment. 

There  is  one  general  consequence  of  these  results  upon 
which  I  should  like  to  dwell  a  moment  longer.  In  a  broad 
sense  the  efforts  of  public  health  and  hygiene  have  been 
directed  against  the  affections  comprised  in  the  first  two 
items  in  the  chart,  those  of  the  respiratory  system  and 
the  alimentary  tract.  The  figures  for  the  two  five-year 
periods  in  the  United  States,  1901-05  and  1906-10,  indi- 
cate roughly  the  rate  of  progress  such  measures  are 
making,  looking  at  the  matter  from  a  broad  biological 
standpoint.  In  reference  to  the  respiratory  system  there 
was  a  decline  of  fourteen  per  cent,  in  the  death  rate  be- 
tween the  two  periods.  This  is  substantial.  It  is  prac- 
tically all  accounted  for  in  phthisis,  lobar  pneumonia  and 
bronchitis.  For  the  alimentary  tract  the  case  was  not 
so  good — indeed  far  worse. 

Between  the  two  periods  the  death  rate  from  this  cause 
group  fell  only  1.8  per  cent.  All  the  gain  made  in  typhoid 
fever  was  a  great  deal  more  than  offset  by  diarrhoea  and 
enteritis  (under  two),  congenital  debility  and  cancer. 
Child  welfare,  both  prenatal  and  postnatal,  seems  by  long 
odds  the  most  hopeful  direction  in  which  public  health 
activities  can  expect,  at  the  present  time,  substantially  to 
reduce  the  general  death  rate.  This  is  a  matter  funda- 
mentally of  education. 

SPECIFIC  DEATH  RATES  BIOLOGICALLY  CLASSIFIED 

Up  to  this  point  in  our  discussions  we  have  been  deal- 
ing with  crude  death  rates,  uncorrected  for  the  age  and 
sex  distributions  of  the  populations  concerned.  It  is, 
of  course,  a  well  known  fact  that  differences  in  age  and 


THE  CAUSES  OF  DEATH  113 

sex  constitution  of  populations  may  make  considerable 
differences  in  crude  death  rates,  in  cases  where  no  real 
differences  in  the  true  force  of  mortality  exist.  What 
is  essential  for  the  further  prosecution  of  the  analysis  of 
the  causes  of  death  is  to  get  specific  death  rates  for  the 
several  causes.  By  an  age  and  sex  specific  death  rate 
is  meant  the  rate  got  by  dividing  the  number  of  persons, 
of  particular  specified  age  and  sex,  dying  from  a  particu- 
lar cause,  by  the  total  number  of  persons  living  in  the 
same  population  of  the  same  age  and  sex.  In  other 
words,  we  need  to  get  as  the  divisor  of  the  rate  fraction 
the  number  of  persons  who  can  be  regarded  as  truly  ex- 
posed to  risk.  This  exposed-to-risk  portion  of  the  popu- 
lation is  never  correctly  stated  in  a  crude  death  rate. 
For  example,  a  person  now  75  years  old  cannot  be  re- 
garded as  exposed  to  risk  of  death  at  age  45.  He  was 
once  exposed  to  that  risk  but  passed  it  safely.  Yet  in  a 
crude  death  rate  he  is  counted  with  those  of  age  45. 

Age  and  sex  specific  death  rates  have  hitherto  been 
available  for  the  American  people,  in  any  general  or  com- 
prehensive form,  only  from  the  extensive  memoir  by 
Dublin,  Kopf  and  Van  Buren,  based  upon  the  mortality 
experience  of  the  Metropolitan  Life  Insurance  Company 
with  its  industrial  policy  holders.  In  a  broad  way,  it 
may  be  said  that  the  data  on  which  the  f  ollo\ving  discus- 
sion is  based,  derived  from  the  general  population  of 
the  Registration  Area,  are  essentially  in  accord  ^vith  those 
of  Dublin  on  a  more  restricted  group.  Owing  to  limita- 
tions of  space,  it  is  not  possible  to  present  all  the  detailed 
rates  here. 

With  the  aid  of  Dr.  William  H.  Davis,  director  of 
vital  statistics  in  the  Census  Bureau,  who  very  kindly 
provided  me  with  the  necessary  unpublished  data,  it  has 

8 


114  BIOLOGY  OF  DEATH 

been  possible  to  calculate  the  specific  death  rates  for  each 
of  the  189  causes  of  death  of  the  International  List,  for 
each  sex  separately,  and  for  each  age  in  5  year  groups, 
for  the  United  States  Registration  Area,  exclusive  of 
North  Carolina,  in  1910.  These  results  have  been  put 
together  in  the  biological  scheme  of  classification  and  may 
be  presented  briefly  in  the  form  of  diagrams. 

The  summary  table  from  which  these  curves  are  plot- 
ted is  given  as  Table  9. 

Let  us  first  consider  deaths  from  all  causes  taken 
together,  in  order  to  recall  to  mind  the  general  form  of 
a  death  rate  curve.  It  will  be  noted,  at  once,  that  the 
rates  are  plotted  along  the  vertical  axis  on  what  strikes 
one  at  first  as  a  peculiar  scale.  The  scale  is  logarithmic. 
The  horizontal  lines  are  spaced  in  proportion  to  the 
logarithms  of  the  numbers  at  their  left,  instead  of  in  pro- 
portion to  the  numbers  themselves.  The  advantages  of 
this  rnethod  of  plotting  in  the  present  case  are  two-fold. 
First,  it  is  possible  to  get  a  much  wider  range  of  values 
on  the  diagram ;  and  second  the  logarithmic  scale  permits 
direct  and  accurate  estimation  of  the  rate  of  change  of  a 
variable.  A  straight  line  forming  an  angle  mth  the  hor- 
izontal on  a  logarithmic  scale  means  that  the  variable 
is  increasing  or  decreasing,  as  the  case  may  be,  at  a  con- 
stant rate  of  change. 

Figure  27  gives  the  specific  death  rates  for  the  com- 
bined total  of  all  causes.  The  curve  in  general  has  the 
form  of  a  V,  with  one  limb  much  extended  and  pulled  over 
to  the  right.  Examining  it  more  in  detail,  we  note  that 
in  the  first  year  of  life,  the  specific  death  rate,  or,  as  we 
may  roughly  call  it,  the  force  of  mortality,  bears  heav- 
ier on  female  infants  than  on  the  males.  Out  of  a  thou- 
sand exposed  to  risk,  124  male  babies  die  in  that  year, 


THE  CAUSES  OF  DEATH 


115 


100  and 
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116 


BIOLOGY  OF  DEATH 


and  143  female.  This  is  the  only  year  of  life  in  which  the 
total  force  of  mortality  is  heavier  among  females  than 
males.     From  that  time  on  to  the  end  of  the  span  of  life, 


tOOOr 


Fig.  27. — Diagram  showing  the  specific  death  rate  at  each  age  for  deaths  from  all  causes 

taken  together. 

the  female  curve  lies,  by  greater  or  less  amounts,  below 
the  male  curve.  After  the  heavy  mortality  of  early 
infancy,  the  curve  drops  in  almost  a  straight  line  to  the 


THE  CAUSES  OF  DEATH  117 

age  period  of  10-15,  where  it  reaches  its  lowest  point,  and 
only  approximately  2-i/^  persons  out  of  a  thousand  ex- 
posed to  risk  die.  The  specific  mortality  curve  then  be- 
gins to  rise,  and  continues  to  do  so  at  an  approximately 
constant  and  rapid  rate  for  ten  years — that  is  to  the 
age  period  20-25.  From  then  on  to  the  age  period  50-55 
it  rises  at  a  slower  but  constant  rate.  This  is  the  period 
of  middle  life,  and  here  the  female  curve  drops  farther 
below  the  male  curve  than  at  any  other  place  in  the  span 
of  life.  After  the  age  period  50-55  with  the  on-coming  of 
old  age,  both  male  and  female  curves  begin  again  to  rise 
more  rapidly.  They  continue  this  rise,  at  a  practically 
constant  rate  of  increase,  to  the  end  of  life,  which  is  here 
taken  as  falling  in  the  age  period  95-100.  In  this  last 
class  the  rate  has  become  very  high.  Out  of  1,000  per- 
sons Living  at  the  ages  of  95  and  100,  and  therefore  ex- 
posed to  risk  of  death  within  that  period,  494  males  and 
473  females  die,  taking  an  average  for  the  whole  five- 
year  period.  Of  course,  before  the  completion  of  the 
period,  practically  all  of  the  thousand  mil  have  passed 
away. 

The  important  things  to  note  about  this  curve  are 
these:  First,  the  highest  specific  forces  of  mortality  oc- 
cur at  the  extreme  ends  of  life,  and  are  higher  at  the 
final  end  than  at  the  beginning.  In  the  second  place, 
there  is  a  sharp  and  steady  drop,  in  almost  a  straight 
line,  from  the  high  specific  force  of  mortality  in  infancy 
to  the  low  point  at  about  the  time  of  puberty.  From 
then  on  to  the  end  of  the  span  of  life,  the  force  of  mortal- 
ity becomes  greater  every  year  at  a  nearly  constant  rate 
of  increase,  with  only  such  slight  deviations  from  this 
constancy  of  rate  as  have  already  been  pointed  out. 

Turning  next  to  the  mortality  of  our  first  biological 


^ 


118 


BIOLOGY  OF  DEATH 


group — namely  deaths  caused  by  breakdoA\Ti  of  the  cir- 
culatory system,  blood  and  blood-forming  organs — we 
note  in  Figure  28  a  marked  difference  in  the  form  of  the 


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AGE. 

Fig.  28. — Diagram  showing  the  specific  death  rate  at  each  age  from  breakdown    of  the 
circulatory  system,  blood  and  blood-forming  organs  (Group  I). 

curve  from  what  we  have  seen  for  the  case  of  all  causes 
of  death.  In  the  first  place,  the  specific  force  of  mortal- 
ity of  this  group  of  causes  is  relatively  low  in  infancy  and 


THE  CAUSES  OF  DEATH  119 

cliildhood.  Out  of  a  thousand  infants  of  each  sex  exposed 
to  risk,  only  7  males  and  5  females  die  from  breakdo^v^l 
of  this  group  of  organs  during  the  first  year  of  life. 
The  trough  of  the  curve  associated  with  the  mortality  r)f 
childhood  and  youth  is  very  much  less  pointed  than  in 
the  case  of  ''all  causes."  It  is  a  smootldy  rounded, 
rather  than  a  sharply  pointed  depression.  It  is  also 
noteworthy  that  between  approximately  the  ages  of  5 
and  35  the  specific  force  of  mortality  from  diseases  of  the 
circulatory  system  and  related  organs  is  higher  for 
females  than  it  is  for  males.  This  condition  of  affairs  is 
probably  connected  with  the  graver  physiological  changes 
and  readjustments  called  forth  by  puberty  in  the  female 
than  accompany  the  same  vital  crisis  in  the  male.  From 
early  adult  life,  say  age  25-30  on,  the  specific  death  rate 
from  diseases  of  the  circulatory  system  and  related  organs 
increases  at  an  almost  absolutely  constant  rate  until  age 
85  is  reached.  After  that,  the  rate  of  increase  slows 
down  somewhat.  Of  those  reaching  the  ages  95-100,  be- 
tween 70  and  80  out  of  each  thousand  living  die  from 
breakdown  of  this  group  of  organs. 

The  specific  mortality  curve  for  deaths  from  break- 
down of  the  respiratory  system,  as  sho\\Ti  in  Figure  29, 
presents  a  number  of  points  of  peculiar  interest.  In 
the  first  place  we  note  that  this  organ  system  is  much 
more  liable  to  breakdo^vn  than  is  the  circulatory  system 
during  all  the  earlier  years  of  life  up  to  about  age  60-65. 
The  decline  in  the  curve  from  the  liigh  point  of  infancy  to 
the  low  point  of  the  period  about  puberty  is  more  sharp 
and  sudden  than  that  of  the  circulatory  system  curve. 
Again, however,  just  as  in  the  former  case, we  note  that  tlie 
specific  force  of  mortality  from  breakdown  of  this  organ 
system  impinges  more  heavily  upon  females  than  upon 


120 


BIOLOGY  OF  DEATH 


males  in  the  years  from  5-20.  This  difference  is  prob- 
ably connected,  as  before,  with  the  greater  physiological 
disturbance  of  puberty  in  the  female  than  in  the  male. 


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O      S      lO      15     ZO    £S    30    35    40    4-5    £0    S5    e>0     C5    70    75    60    65    90    95     lOO 

AGE 

Fig.   29. — Diagram  showing  the  specific  death  rate  at  each  age  from  breakdown  of  the 

respiratory  system  (Group  II). 

The  lowest  point  of  the  respiratory  curve  falls  in  the 
age  group  10-15.  Between  the  ages  25-70  there  is  a  very 
striking  difference  in  the  two  sexes  in  respect  of  specific 


THE  CAUSES  OF  DEATH  121 

mortality  from  breakdo^vn  of  the  respiratory  system. 
The  male  curve  rises  in  nearly  a  straight  line,  while  the 
female  curve  lies  far  below  it,  and  actually  show\s  a  point 
of  inflection  at  about  age  45,  becoming  for  a  slK)rt  period 
convex  to  the  base.  The  explanation  for  the  great  sep- 
aration of  the  two  curves  in  this  period  is  probably  fun- 
damentally occupational.  From  the  nature  of  their 
activity  males,  during  this  period  of  life,  are  probably 
subject  to  a  greater  risk  of  breakdo^vn  of  the  respiratory 
system  than  are  the  more  protected  female  lives.  From 
age  70  on,  both  curves  ascend  with  increased  rapidity, 
the  female  curve  rising  above  the  male,  presumably  in 
compensation  for  the  marked  dip  which  it  exhibits  in  mid- 
dle life.  It  is,  of  course,  well  known  that  respiratory 
mortality  bears  heavily  upon  the  aged. 

The  next  group  which  we  shall  consider  has  to  do 
with  deaths  from  breakdown  of  the  primar^^  and  second- 
ary sex  organs.  This  cause  group  furnishes  an  ex- 
tremely interesting  pair  of  curves  shown  in  Figure  30. 
Before  discussing  in  detail  their  form,  a  word  of  explan- 
ation as  to  their  makeup  should  be  given.  This  may 
best  be  done  by  exhibiting  and  discussing  for  a  moment 
the  causes  of  death  which  are  included  in  this  group. 
Table  10  shows  the  data. 

In  this  rubric  are  included  *' Premature  birth"  and 
** Injuries  at  birth."  The  question  at  once  arises,  why 
should  these  two  items,  *^ Premature  birth"  and  ''Injuries 
at  birth"  be  included  with  the  primary  and  secondary  sex 
organs,  since  it  is  obvious  enough  that  the  infants  whose 
deaths  are  recorded  under  these  heads  in  the  vast  major- 
ity of  cases,  if  not  all,  have  notliing  whatever  the  matter 
with  either  their  primaiy  or  secondary  organs?  The 
answer  is,  in  general  terms,  that  on  any  proper  biological 


122 


BIOLOGY  OF  DEATH 


basis,  death  coming  under  either  of  these  two  categories  is 
not  properly  chargeable,  organically,  against  the  infant  at 


No. 


151* 

42 

137 

152* 

43 

37 

126 

132 

129 
134 
130 
136 
140 
131 
135 
125 

38 
128 

127 

133 

139 


TABLE  10 

Primary  and  secondary  sex  organs 


"  Cause  of  Death"  as  per  International 
Classification 


Premature  birth 

Cancer  of  the  female  genital  organs 

Puerperal  septicemia 

Injuries  at  birth 

Cancer  of  the  breast 

Syphilis 

Diseases  of  the  prostate 

Salpingitis  and  other  diseases  of 
9  genital  organs 

Uterine  tumor  (non-cancerous)  .  .  . 

Accidents  of  pregnancy 

Other  diseases  of  the  uterus 

Other  accidents  of  labor 

Following  childbirth 

Cysts  and  other  tumors  of  ovary . . 

Puerperal  hemorrhage 

Diseases  of  the  urethra,  urinary 
abscesses,  etc 

Gonococcus  infection 

Uterine  hemorrhage  (non-puerpe- 
ral)   

Non-venereal  diseases  of  cT  genital 
organs 

Non-puerperal  diseases  of  breast 
(except  cancer) 

Puerperal  phlegmasia,  etc 


Totals 


Registration  Area, 
U.  S.  A. 


1906-10 


35.7 
10.8 
6.8 
6.6 
6.5 
5.4 
3.4 

2.2 
1.8 
1.7 
1.6 
1.3 
1.1 
1.0 
1.0 

0.4 
0.3 

0.2 

0.1 

0.1 
0.1 


88.1 


1901-05 


30.8 
10.0 
6.3 
5.0 
5.6 
4.1 
2.6 

2.1 
1.8 
1.7 
1.7 
0.9 
1.5 
1.3 
1.0 

0.4 
0.1 

0.3 

0.1 

0.1 


England 

and 

Wales 

1914 


46.9 

12.9 
3.7 

2.8 

10.4 

5.8 

4.2 

0.5 
0.8 
1.1 
0.4 
1.1 
0.1 
0.8 
1.3 

1.2 
0.2 

0 

0.2 

0.1 
0.9 


77.4       95.4 


Sao 

Paulo 

1917 


66.8 
6.5 
6.5 
2.1 
1.5 

15.0 
0.7 

0.2 

0 

0.2 

0.4 

0.7 


0.2 
1.7 

0.7 
0 


0 

0 

0 
0 


103.2 


*  In  part. 

all,  but  should  be  charged,  on  such  a  basis,  against  the 
mother.  To  go  further  into  detail,  it  is  apparent  that  when 
a  premature  birth  occurs  it  is  because  the  reproductive 


THE  CAUSES  OF  DEATPI  123 

system  of  the  mother, for  some  reason  or  other,  did  not  rise 
to  the  demands  of  the  situation  of  carrying  the  fa^tus  to 
term.  Premature  birth,  in  short,  results  from  a  fail- 
ure or  breakdown  in  some  particular  of  the  maternal 
reproductive  system.  This  failure  may  be  caused  in 
various  ways,  which  do  not  here  concern  us.  The  essential 
feature  from  our  present  viewpoint  is  that  the  reproduc- 
tive system  of  the  mother  does  break  down,  and  by  so 
doing  causes  the  death  of  the  infant,  and  that  death  is 
recorded  statistically  under  this  title  ^^  Premature  birth. '^ 
The  death  organically  is  chargeable  to  the  mother. 

A  considerable  number  of  cases  of  premature  birth 
are  unquestionably  due  to  placental  defects  and  the  pla- 
centa is  a  structure  of  foetal  origin,  so  such  deaths  could 
not  be  properly  charged  to  the  mother.  On  the  other 
hand,  however,  they  would  still  stay  in  the  same  table  be- 
cause the  placenta  may  fairly  be  regarded  as  an  organ 
intimately  concerned  in  reproduction. 

The  same  reasoning  which  applies  to  premature  births, 
mutatis  ynutandiSj  applies  to  the  item  ^^ Injuries  at  birth." 
An  infant  death  recorded  under  this  head  means  that 
some  part  of  the  reproductive  mechanism  of  the  mother, 
either  structural  or  functional,  failed  of  normal  per- 
formance in  the  time  of  stress.  Usually  *^ injury  at 
birth"  means  a  contracted  or  malformed  pelvis  of  the 
mother.  But  in  any  case  the  death  is  purely  external  and 
accidental  from  the  standpoint  of  the  infant.  It  is  organ- 
ically chargeable  to  a  defect  of  the  sex  organs  of  the 
mother.  The  female  pelvis,  in  respect  of  its  conforma- 
tion, is  a  secondary  sex  character. 

The  immediate  reason  for  including  syphilis  and 
gonococcus  infection  here  is  obvious,  but,  particularly  in 
relation  to  syphilis,  the  point  needs  further  discussion. 


124  BIOLOGY  OF  DEATH 

As  a  cause  of  actual  death,  syphilis  frequently  acts 
through  the  central  nervous  system,  and  the  question  may 
fairly  be  raised  why,  in  view  of  this  fact,  syphilis  is  not 
tabled  there.  The  point  well  illustrates  one  of  the  fun- 
damental difficulties  in  any  organological  classification 
of  disease.  In  the  case  of  syphilis,  however,  the  difficulty 
in  practice  is  not  nearly  so  great  as  it  is  in  theory.  As 
a  matter  of  fact,  most  of  the  deaths  from  the  effect  of 
syphilitic  infection  on  the  nervous  system  are  recorded 
in  vital  statistics  by  reporting  physicians  and  vital  statis- 
ticians as  diseases  of  the  nervous  system.  For  example, 
it  is  perfectly  certain  that  most  of  the  deaths  recorded 
as  due  to  **  locomotor  ataxia '^  are  fundamentally  syphil- 
itic in  origin.  The  rate  of  5.4  for  the  Registration  Area 
of  the  United  States  in  1906-10  for  deaths  due  to  syphilis 
is  far  lower,  as  any  clinician  knows,  than  the  number  of 
deaths  really  attributable  to  syphilitic  infection.  These 
other  deaths,  due  to  syphilis,  and  not  reported  under  that 
title,  are  reported  under  the  organ  which  primarily 
breaks  down  and  causes  death,  as,  for  example,  the  brain, 
and  will  in  the  present  system  of  classification  be  included 
under  the  nervous  system.  After  careful  consideration, 
it  has  seemed  as  fair  as  anything  which  could  be  done  to 
put  the  residue  of  deaths  specifically  reported  as  due 
to  syphilis  under  Primary  and  Secondary  Sex  Organs. 
The  rate,  in  any  event,  is  so  smaU  that  whatever  shift  was 
made  could  not  sensibly  affect  the  general  results  to 
which  we  shall  presently  come. 

Turning  now  to  the  consideration  of  Figure  30,  which 
gives  the  curves  of  specific  mortality  from  breakdown  of 
the  reproductive  organs,  we  note  at  once  the  high  specific 
death  rate  of  infants  under  one,  recorded  by  the  female 
line.     This  rate  is  over  40  per  thousand  exposed  to  risk. 


THE  CAUSES  OF  DEATH 


125 


o 


It  includes,  of  course,  both  male  and  female  infants,  dy- 
ing from  congenital  debility,  premature  birth  and  injuries 
at  birth,  because,  according  to  the  reasoning  just  exphiined. 


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01 


0  01 


PPIMARY    AND    SECONDARY     SEX      ORGANS 


FiQ.  30. — Diagram  showing  specific  death  rates  at  each  acre  from  breakdown  of  the  primary 

and  secondary  sex  organs  (Group  III). 

these  deaths  are  organically  chargeable  to  breakdo^^^l  or 
failure  to  function  properly  of  the  reproductive  organs 
of  the  mother.     These  deaths,   therefore,  go   into   the 


126  BIOLOGY  OF  DEATH 

female  group.     By  the  fifth  year  of  life,  the  specific  rates 
of   mortality   chargeable   to   reproductive    organs   have 
dropped  in  both  sexes  practically  to  zero,  amounting  to 
less  than  0.01  per  thousand  exposed  to  risk.     At  about 
the  time  of  puberty  the  female  curve  begins  to  rise  and 
goes  up  very  steeply.     By  age  30  it  has  reached  a  value 
of  1  per  thousand  exposed  to  risk.     From  that  point  the 
force  of  this  specific  mortality  rises  slowly,  but  at  a 
practically  constant  rate,  to  extreme  old  age.     The  male 
curve  is  in  striking  contrast  to  the  female.     From  about 
age  20  it  rises  steadily,  at  an  almost  constant  rate  of 
increase,  but  a  much  slower  one  than  the  female,  until 
the  end  of  the  life  span.     It  crosses  the  female  curve — in- 
dicating a  higher  specific  rate  of  mortality  from  break- 
down of  the  reproductive  organs  in  men  than  in  women — 
for  the  first  time  at  about  age  78.     This  is,  of  course,  the 
time  of  life  when  disturbed  functioning  of  the  prostate 
gland  in  the  male  begins  to  take  a  relatively  hea\"y  toll. 
Figure   31   shows   specific   rates   of  mortality  from 
breakdoAvn  of  the  kidneys  and  related  excretory  organs. 
Death  from  these  causes  is  relatively  infrequent  in  in- 
fancy and  early  childhood.     The  low  point  is  reached, 
as  in  so  many  of  the  other  cases,  at  about  the  time  of 
puberty.     From  then  on  practically  to  the  end  of  the 
span  of  life  the  specific  force  of  mortality  from  excretory 
failure  increases  at  an  almost  constant  rate.     During 
the  reproductive  period,  from  about  15  to  45  years  of  age, 
specific  rates  of  mortality  from  these  causes  are  higher 
in  the  female  than  in  the  male.     After  that  point  the  male 
curve  is  higher.     The  relatively  heavy  specific  mortality 

of  the  female  in  early  life  is  undoubtedly  due  to  the  hea\^ 

strain  put  upon  her  excretory  organs  by  child-bearing. 

The  specific  force  of  mortality  from  breakdo^vn  of 


THE  CAUSES  OF  DEATH 


127 


the  skeletal  and  muscular  systems,  shown  in  Fitrure  32, 
presents  an  interesting  pair  of  curves.  Throughout  the 
span  of  life  there  is  practically  no  difference  between 


lOO 


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Fia.  31. — Diagram  showing  specific  death  rates  at  each  age  from  breakdown  of  the  kidne>'B 

and  related  excretory  organs  (Group  IV). 

the  female  and  male  in  the  incidence  of  this  mortality, 
the  curves  ^vdnding  in  and  out  about  each  otlier.  The 
striking  characteristics  of  the  curve  are:  first,  that  the 
specific  forces  of  mortality  are  nbsolutoly  low  for  those 


128 


BIOLOGY  OF  DEATH 


organ  systems;  and  second,  that  the  minimum  point  is 
reached  not,  as  in  most  of  the  other  cases,  around  the  time 
of  puberty,  but  at  a  much  later  period — namely  in  the 


too 


O      -5     10     15     ZO    Z-5    3Q    35   40   45    50    55    60    65    10     15    60    Q5    90  35    lOO 

AGE. 

Fig.  32. — Diagram  showing  specific  death  rates  at  each  age  from  breakdown  of  the  skeletal 

and  muscular  systems  (Group  V). 

late  twenties.     The  whole  curve  shows  a  very  gradual 
change  in  the  rates. 

The  next  diagram,  Figure  33,  shows  one  of  the  most 


THE  CAUSES  OF  DEATH 


129 


significant  organ  groups  in  the  force  of  its  specific  mor- 
tality. Breakdo^vn  and  failure  to  function  properly  of 
the  primary  organs  of  metabolism — the  organs  which 


100 


5 


Si 


f 

§ 


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Fig.  33. — Diagram  showing  the  specific  rates  of  death  at  each  age  from  breakdown  of  the 
alimentary  tract  and  associated  organs  of  metabolism  (Group  VI). 

transform  the  fuel  of  the  human  machine  into  vital  energy 
— occur  with  relatively  hea\^  frequency  at  all  periods 
of  life.     These  curves  are  among  the  few  which  show  au 
9 


130 


BIOLOGY  OF  DEATH 


absolutely  higher  specific  force  of  mortality  in  infancy 
than  in  extreme  old  age.  There  is  practically  no  signif- 
icant difference  between  the  male  and  female  curve  at 


100 


\ 


OOi 


Fia.    34. — Diagram  showing  the  specific  death  rates  at  each  age  from  breakdown  of  the 

nervous  sj'stem  and  sense  organs  (Group  VII). 

any  portion  of  life.  During  early  adult  life  the  female 
cur\^e  lies  below  the  male,  but  by  only  a  small  amount. 
Out  of  every  thousand  infants  under  one,  about  sixty 


THE  CAUSES  OF  DEATH  131 

die  in  the  first  year  of  life  from  breakdown  of  the  ali- 
mentary tract  and  its  associated  organs.  After  the  low- 
point,  wliich  falls  in  the  relatively  early  period  of  7  to  12 
years  of  age,  there  is  a  rapid  rise  for  about  ten  years 
in  the  specific  rates  of  mortality,  followed  by  a  slowing 
off  in  the  rate  of  increase  for  the  next  ten  or  fifteen  years, 
after  which  point  the  curve  ascends  at  a  practically  uni- 
form rate  until  the  end  of  the  span  of  life. 

Figure  34  shows  the  trend  of  the  specific  mortality 
from  breakdowTi  of  the  nervous  system  and  sense  organs. 
This  organ  group,  on  the  whole,  functions  very  well,  giv- 
ing a  relatively  low  rate  of  mortality  until  toAvards  the 
end  of  middle  life.  Then  the  specific  rates  get  fairly 
large.  The  low  point  in  tliis  curve  is,  as  in  most  of  the 
others,  at  about  the  time  of  puberty.  From  then  on  to 
the  end  of  the  life  span  the  specific  rates  increase  at  a 
practically  uniform  rate.  The  female  curve  everywhere 
lies  below"  the  male  curve  except  at  the  extreme  upper 
end  of  the  life  span.  Before  that  time,  and  particularly 
between  the  ages  of  20  and  50,  the  business  of  living 
evidently  either  imposes  no  such  heavy  demand  on  the 
nervous  system  of  the  female  as  it  does  on  that  of  the 
male,  or  else  the  nervous  system  of  the  female  is  organi- 
cally sounder  than  that  of  the  male.  The  former  sug- 
gestion seems  the  more  probable. 

That  breakdo^^^l  and  failure  to  function  properly,  of 
the  skin  as  an  organ  system,  is  a  relatively  insignificant 
factor  in  human  mortality,  is  demonstrated  by  Figure  35. 
From  a  specific  death  rate  of  about  1  per  thousand  in 
the  first  year  of  life  it  drops  abruptly,  practically  to  zero, 
in  early  childhood.  At  about  the  time  of  puberty  it  be- 
gins to  rise  again,  and  ascends  at  a  steady  rate  during 
all  the  remainder  of  life.     The  final  high  point  reached 


132 


BIOLOGY  OF  DEATH 


is  absolutely  low,  however,  amounting  to  a  specific  death 
rate  among  those  exposed  to  risk  of  only  a  little  more  than 
4  per  thousand  at  the  extreme  end  of  life.     The  female 


lOO 


Fig.   35. — Diagram  showing  the  specific  death  rates  at    each  age  chargeable  against  the 

skin  (Group  VIII). 

curve  lies  well  below  the  male  curve  practically  through- 
out its  course. 

Deaths  from  failure  to  function  properly  of  the  organs 


THE  CAUSES  OF  DEATH 


133 


of  the  endocrinal  system,  including  the  thyroid  gland, 
suprarenal  glands,  etc.,  do  not  become  significant  until 
middle  life  in  the  case  of  the  male,  as  sho^v^l  in  Figure  3G, 


lOO 


10 


3y 


2-§ 


ENDOCRINAL     3VSTEA1 


OOl 


Fia.  36.— Diagram  showing  the  specific  death  rates  at  each  age  from  breakdown  of  the 

endocrinal  system  (Group  IX). 

although  in  the  female  the  curve  begins  to  rise  from  pu- 
berty on.  The  specific  rates  at  all  ages,  of  course,  are 
extremely  small,  practically  never  rising  to  more  than 


134 


BIOLOGY  OF  DEATH 


1/10  of  one  person  per  thousand  exposed  to  risk.  The 
well-known  fact  that  these  glandular  organs,  whose  se- 
cretions are  so  important  for  the  normal  conditions  of 


i.0O0rz 


FiQ.   37. — Diagram  showing  the  specific  death  rates  from  all  other  causes  of  death  not 

covered  in  the  preceding  categories  (Group  X). 

life,  are  much  more  unstable  and  liable  to  breakdown 
in  the  female  than  in  the  male,  is  strikingly  shown  by 
this  diagram. 


THE  CAUSES  OF  DEATH  135 

Finally,  we  have  the  diagram  for  our  omnium  gatherum 
group,  the  ''All  other  causes  of  death,''  in  Figure  37. 
Here  we  see  that,  because  of  accidental  and  violent  deaths, 
the  male  specific  mortality  curve  lies  far  above  the 
female,  from  youth  until  old  age  has  set  in,  a])out  age  75. 
From  that  point  on  to  the  end  of  the  span  of  life  both 
curves  ascend  rapidly  together,  as  a  result  of  the  deaths 
recorded  as  resulting  from  senility.  Eventually  it  is 
to  be  expected  that  no  deaths  will  be  registered  as  result- 
ing from  senility.  We  shall  have  them  all  put  more  nearly 
where  they  belong. 

These  diagrams  of  specific  forces  of  mortality  give 
altogether  a  remarkably  clear  and  definite  picture  of  how 
death  occurs  among  men.  We  see  that  failure  of  certain 
organ  systems,  such  as  the  lungs,  the  heart,  the  kidneys, 
to  maintain  their  structural  and  functional  integrity,  has 
an  overwhelmingly  great  effect  in  determining  the  total 
rate  of  mortality  as  compared  with  some  of  the  other 
organ  systems.  One  cannot  but  be  impressed,  too,  with 
the  essential  orderliness  of  the  phenomena  we  have  ex- 
amined. The  probability  of  any  particular  organ  system 
breaking  down  and  causing  death  is  mathematically  def- 
inite at  each  age,  and  changes  in  a  strikingly  orderly 
manner  as  age  changes,  as  is  sllo^^^l  in  Table  11.  Thus 
we  find  that  in  the  first  year  of  life  it  is  the  alimentary 
tract  and  its  associated  organs  which  most  frequently 
break  down  and  cause  death.  From  age  1  to  age  60 
the  specific  force  of  mortality  from  breakdown  of  the 
respiratory  system  is  higher  (with  a  few  insignificant 
exceptions  in  the  females)  usually  by  a  considerable 
amount,  than  that  associated  with  anv  other  onran  svstem 
of  the  body.     From  60  to  90  years  of  age  the  circulatory 


136 


BIOLOGY  OF  DEATH 


system  takes  the  front  rank,  with  a  higher  specific  mor- 
tality rate  than  any  other  organ  system. 

TABLE  11 

The  most  fatal  organ  systems  at  different  ages 


MALES 

Age 
Group 

FEMALES 

Per  cent,  of  all 

biologically 

classifiable 

deaths  due  to 

breakdown  of 

specified  organ 

system 

Organ  system 

concerned  in  largest 

proportion 

of  fatalities 

Organ  system 

concerned  in  largest 

proportion 

of  fatalities 

Per  cent,  of  all 

biologically 

classifiable 

deaths  due  to 

breakdown  of 

specified  organ 

sj'stem 

68.8 

Alimentary  tract 

0—  1 

Alimentary  tract 

40.6 

50.1 

Respiratory 

1—  4 

Respiratory 

51.3 

41.2 

Respiratory- 

5—  9 

Respiratory 

42.5 

27.1 

Respiratory 

10—14 

Respiratory 

33.3 

43.6 

Respiratory 

15—19 

Respiratory 

43.8 

52.6 

Respiratory 

20—24 

Respiratory 

46.0 

49.7 

Respiratory 

25—29 

Respiratory 

44.2 

45.6 

Respiratory 

30—34 

Respiratory 

39.5 

39.9 

Respiratory 

35—39 

Respiratory 

33.2 

33.3 

Respiratory 

40—44 

Respiratory 

27.5 

28.0 

Respiratory 

45—49 

Respiratory- 

22.1 

23.6 

Respiratory 

50—54 

Alimentary  tract 

21.6 

25.0 

Circulatory 

55—59 

Alimentary  tract 

22.6 

28.4 

Circulatory 

60—64 

Circulatory 

24.4 

30.9 

Circulatory 

65—69 

Circulatory 

25.6 

32.5 

Circulatory 

70—74 

Circulatory 

28.0 

32.9 

Circulatory 

75—79 

Circulatory 

28.4 

33.3 

Circulatory 

80—84 

Circulatory 

30  4 

85—89 

Circulatory 

30.8 

If  our  lungs  were  as  organically  good  relatively  as 
our  hearts,  having  regard  in  each  case  for  the  work  the 
organ  is  called  upon  to  do  and  the  conditions  under  which 
it  must  do  it,  we  should  live  a  considerable  number  of 
years  longer  on  the  average  than  we  do  now.  One  cannot 
but  feel  that  the  working  out  of  a  rational  and  scientifi- 
cally grounded  system  of  personal  hygiene  of  the  respir- 


THE  CAUSES  OF  DEATH  137 

atory  organs,  on  the  broadest  basis,  to  include  all  sucli 
matters  as  ventilation  of  buildings,  etc.,  and  the  putting 
of  such  a  personal  hygiene  into  general  use  through 
education,  would  pay  about  as  large  di\adends  as  could 
be  hoped  for  from  any  investment  in  public  health  secu- 
rities. I  am  aware  that  much  has  alreadv  Ix^eii  done  in 
this  direction,  but  in  order  to  reap  any  such  dividends 
as  I  am  thinking  of,  a  vast  amount  must  be  added  to  our 
present  knowledge  of  the  physiology,  pathology,  epidemi- 
ology, and  every  other  aspect  of  the  functions  and  struc- 
tures of  respiration. 


CHAPTER  V 
EMBRYOLOGY  AND  HUMAN  MORTALITY 

In  the  preceding  chapter  attention  was  confined 
strictly  to  the  organological  incidence  of  death.  It  is 
possible  to,  push  the  matter  of  human  mortality  still 
farther  back.  In  the  embryological  development  of  the 
vertebrate  body,  there  are  laid  down  at  an  early  stage, 
in  fact  immediately  f ollo^\ang  the  process  of  gastrulation, 
three  morphologically  definite  primitive  tissue  elements, 
called  respectively  the  ectoderm,  the  mesoderm  and  the 
endoderm.  These  are  termed  the  germ-layers,  and  em- 
bryological science  has,  for  a  great  many  forms,  succeeded 
in  a  broad  way  in  tracing  back  to  the  primitive  germ 
layer  from  which  it  originally  started  its  development, 
substantially  every  one  of  the  adult  organs  and  organ 
systems  of  the  body.  It,  makes  no  difference  to  the  validity 
or  significance  of  the  discussion  which  we  are  about  to  enter 
upon,  in  what  degree  of  esteem  or  contempt  in  biological 
philosophy  the  germ  layer  theory  or  doctrine,  which  oc- 
cupied so  large  a  place  in  morphological  speculation  50 
years  ago,  may  be  held.  We  are  here  concerned  only  mth 
the  well-established  broad  descriptive  fact,  that  in  general 
all  adult  organ  systems  may  be  traced  back  over  the  path 
of  their  embryological  development  to  the  germ  layer,  or 
combination  of  germ  layers,  from  which  they  origin- 
ally started. 

Having  arranged,  so  far  as  possible,  all  causes  of  death 
on  an  organological  basis,  it  occurred  to  me  to  go  one 

138 


EMBRYOLOGY  AND  HUMAN  MORTALITY  130 

step  further  back  and  combine  them  under  the  headings 
of  the  primary  germ  layers  from  wliicli  tlie  several  organs 
developed  embryologically.  To  do  tliis  was  a  task  of 
considerable  difficulty.     It  raised  intricate,  and  in  some 

TABLE  12 

Showing  the  relative  influence  of  the  primary  germ  layers  in  human  mortality 

(Items  64  and  65  charged  to  ectoderm) 


Locality 

Death  rate  per  100,000  due  to  functional  breakdown 
of  organs  embryologically  developing  from 

Ecto- 
derm 

Per 
cent. 

MeBO- 
derm 

Per 

cent. 

Endo- 
derm 

Per 

cent. 

United  States  Registration 
Area,  1906-10 

191.1 

210.6 
177.1 
134.9 

14.3 

15.0 
14.4 

8.4 

425.2 

407.1 
374.0 
468.0 

31.8 

29.0 
30.3 
29.0 

719.6 

786.2 

681.5 

1009.9 

53.9 

United  States  Registration 
Area,  1901-05 

56.0 

England  and  Wales,  1914.  . . 
Sao  Paulo,  1917 

55.3 
62.6 

TABLE  13 

Showing  the  relative  influence  of  the  primary  germ  layers  in  human  mortality 

(Items  64  and  65  charged  to  mesoderm) 


Locality 

Death  rate  per  100,000  due  to  functional  breakdown 
of  organs  embryologically  developing  from 

Ecto- 
derm 

Per 

cent. 

Meso- 
derm 

Per 

cent. 

Endo- 
derm 

Per 
cent. 

United  States  Registration 
Area,  1906-10 

116.9 

137.3 
107.9 
101.3 

8.7 

9.8 
6.7 
6.3 

499.4 

480.4 
443.2 
501.6 

37.4 

34.2 
36.0 
31.1 

719.6 

786.2 

681.5 

1009.9 

53.9 

United  States  Registration 
Area,  1901-05 

56  0 

England  and  Wales,  1914.  . . 
Sao  Paulo,  1917 

55.3 
62.6 

cases  still  unsettled,  questions  of  embryology.  Further- 
more, the  original  statistical  rubrics  under  whicli  the  data 
are  compiled  by  registrars  of  vital  statistics  were  never 
planned  with  such  an  object  as  this  in  mind.  Still  the  thing 
seemed  worth  trying  because  of  the  biological  interest 
which  would  attach  to  the  result,  even  though  it  were  some- 


140 


BIOLOGY  OF  DEATH 


what  crude  and,  in  respect  of  minor  and  insignificant 
details,  open  to  criticism.  It  is  not  possible  here  to  go  into 
details  as  to  how  the  causes  of  death  were  combined  in 


53.5 
53.9 


US.  REGlSTR/iT/ON  AREA       1906 'iO 


ENGLAND    and     VJALES        191'^ 


ea.e 
6^.6 


SAO    PAULO       J917 


^ 


END0D5RM 


MESODERM 


ECTODERM 


Fig.  38. — Diagram  showing  the  percentages  of  biologically  classifiable  human  mortality 
resulting  from  breakdown  of  organs  developing  from  the  different  germ  layers.  Upper  bar 
of  pair  gives  upper  limit  of  mortaUty  chargeable  to  ectoderm:  lower  bar  gives  lower  limit  of 
mortaUty  chargeable  to  ectoderm. 

making  up  the  final  tables.     For  these  details  one  must 
refer  to  the  original  papers. 

Tables  12  and  13,  and  Figure  38,  give  the  results  for 
the  crude  mortality  of  the  U.  S.  Eegistration  Area,  Eng- 
land and  Wales,  and  Sao  Paulo,  Brazil. 


EMBRYOLOGY  AND  HUMAN  MORTALITY  141 

The  figures  show  that  in  man,  the  hi^^hest  product  of 
organic  evolution,  about  57  per  cent,  of  all  the  biolo^-ically 
classifiable  deaths  result  from  a  breakdown  and  faihire 
further  to  function  of  organs  arising  from  tlie  endoderm 
in  their  embryological  development,  while  but  from  8 
per  cent,  to  13  per  cent,  can  be  regarded  as  a  result  of 
breakdown  of  organ  systems  arising  from  the  ectoderm. 
The  remaining  30  to  35  per  cent,  of  the  mortality  results 
from  failure  of  mesodermic  organs.  The  two  values 
stated  for  ectoderm  and  mesoderm,  shown  by  the  two 
bars  in  the  diagram,  differ  by  virtue  of  the  fact  that  two 
important  causes  of  death,  cerebral  hemorrhage  and 
apoplexy,  and  softening  of  the  brain,  are  put  in  the 
one  case  with  the  ectoderm  and  in  the  other  case  with 
the  mesoderm.  The  pathological  arguments  for  the  one 
disposition  as  against  the  other  of  these  two  diseases  are 
interesting,  but  lack  of  space  prevents  their  exposition 
here.  I  have  chosen  rather  to  present  the  facts  in 
both  ways. 

Taking  a  general  view  of  comparative  anatomy  and 
embryology  it  is  evident  that  in  the  evolutionary  history 
through  which  man  and  the  higher  vertebrates  have  passed 
it  is  the  ectoderm  which  has  been  most  widely  differ- 
entiated from  its  primitive  condition,  to  the  validity  of 
which  statement  the  central  nervous  system  furnishes  the 
most  potent  evidence.  The  endoderm  has  been  least  pro- 
gressively changed  structurally  and  functionally  in  the 
process  of  evolution,  while  the  mesoderm  occupies,  on  the 
whole,  an  intermediate  position  in  this  respect. 

Degree  of  differentiation  of  organs  in  evolution  im- 
plies degree  of  adaptation  to  environment.  From  the  pre- 
sent point  of  view  we  see  that  the  germ  layer,  the  endo- 
derm, which  has  evolved  or  become  differentiated  least  in 


142  BIOLOGY  OF  DEATH 

the  process  of  evolution  is  least  able  to  meet  successfully 
the  vicissitudes  of  the  environment.     The  ectoderm  has 
changed  most  in  the  course  of  evolution.     Of  this  the  cen- 
tral nervous  system  of  man  is  the  best  proof.     There 
have  also  been  formed  in  the  process  of  differentiation, 
protective  mechanisms,  the  skull  and  vertebral  column, 
which  very  well  keep  the  delicate  and  highly  organized 
central  nervous  system  away  from  direct  contact  with 
the  environment.     The  skin  also  exliibits  many  differen- 
tiations of  a  highly  adaptive  nature  to  resist  environmen- 
tal difficulties.     It  is  then  not  surprising  that  the  organ 
systems  developed  from  the  ectoderm  break  down  and 
lead  to  death  less  frequently  than  any  other.     The  fig- 
ures make  it  clear  that  man's  greatest  enemy  is  his  own 
endoderm.     Evolutionally   speaking,   it  is    a  very   old- 
fashioned  and  out-of-date  ancestral  relic,  which  causes  him 
an  infinity  of  trouble.     Practically  all  public  health  ac- 
tivities are  directed  towards  overcoming  the  difficulties 
which  arise  because  man  carries  about  this  antediluvian 
sort  of  endoderm.     We  endeavor  to  modifv  the  environ- 
ment,  and  soften  its  asperities  down  to  the  point  where 
our  own  inefficient  endodermal  mechanism  can  cope  with 
them,  by  such  methods  as  preventing  bacterial  contam- 
ination of  water,  food  and  the  like,  warming  the  air  we 
breathe,  etc.     But  our  ectoderm  requires  no  such  exten- 
sive amelioration  of  the  environment.     There  are  at  most 
only  a  very  few,  if  any,  germs  which  can  gain  entrance  to 
the  body  through  the  normal,  healthy  unbroken  skin. 
We  do,  to  be  sure,  wear  clothes.     But  it  is  at  least  a  debat- 
able question  whether,  upon  many  parts  of  the  earth's 
surface,  we  should  not  be  better  off  without  them  from 
the  point  of  view  of  health. 

These  data  indicate  further  in  another  manner  how 


EMBRYOLOGY  AND  HUMAN  MORTALITY  1 13 

important  are  the  rundameutal  em])ry()locri(.ai  factors 
in  determiiiiii«^-  the  mortality  of  man.  (Jf  the  tliree  hmal- 
ities  compared,  Enjj;land  and  tlie  United  States  may  he 
fairly  regarded  as  much  more  advanced  in  matter's  of 
public  health  and  sanitation  than  Sao  Paulo.  This  fact 
is  reflected  with  perfect  precision  and  justice  in  the  re- 
lative proportion  of  the  death  rates  from  endoderm  and 
ectoderm.  In  the  United  States  and  England  about  f).') 
per  cent,  of  the  classifiable  deaths  are  chargea])Ie  to  endo- 
derm and  about  9  to  14.5  per  cent,  to  ectoderm.  In  Sao 
Paulo  62.6  per  cent,  fall  with  the  endoderm,  and  but  6.3 
to  8.4  per  cent,  with  the  ectoderm.  Since  public  health 
measures  can  and  do  affect  practically  only  the  death 
rate  chargeable  to  endoderm,  this  result,  wliich  is  actually 
obtained,  is  precisely  that  which  would  be  expected. 

A  question  which  naturally  occurs  is  as  to  what  the 
age  distribution  of  breakdo^vn  of  ectodermic,  mesoder- 
mic,  or  endodermic  organs  may  be.  Are  the  endodermic 
organs,  for  example,  relatively  more  liable  to  breakdown 
in  early  life,  and  less  so  later,  as  general  observation 
would  lead  one  to  conclude? 

To  answer  this  and  similar  questions  which  come  to 
mind  it  is  necessary  to  distribute  the  specific  rates  of 
Table  9  upon  an  embryological  basis. 

In  Figure  39  the  result  of  doing  this  is  shown  for 
males.  We  note  that  prior  to  age  60  the  curve  for  the 
breakdow^n  of  organs  of  endodermic  origin  lies  at  the 
top  of  the  diagram;  next  below  it  comes  the  curve  for 
the/  breakdo^vn  of  organs  of  mesodermic  'origin;  and 
finally  at  the  bottom  the  curve  for  the  breakdown  of  or- 
gans of  ectodermic  origin.  All  three  of  the  curves  have 
in  general  the  form  of  a  specific  death  rate  curve.  The 
rates  for  all  three  germ  layers  are  relatively  high  in  in- 


144 


BIOLOGY  OF  DEATH 


fancy  and  drop  at  a  practically  constant  rate  to  a  low 
point  in  early  youth.  In  infancy  the  heaviest  mortality 
in  males  is  due  to  the  breakdown  of  organs  of  endodermic 


1000  rz 


100 


0     5     JO    13    20  25  30   35  AO   ^5    50   55  60    65    70    75    30   35  SO   95   lOO 

AGE 

Fig.  39. — Showing  specific  death  rates  in  males  according  to  the  germ  layer  from  which  the 

organs  developed. 

origin.  This  part  of  the  death  rate  accounts  for  some- 
thing like  10  times  as  many  deaths  as  either  mesoderm  or 
ectoderm  at  this  period  of  life.     From  about  age  12  on  in 


EMBRYOLOGY  AND  HUMAN  MORTALITY  145 

the  case  of  organs  of  ectodermic  origin,  and  from  about 
age  22  on  in  cases  of  mesodermic  origin,  the  death  rate 
curves  rise  at  a  practically  constant  rate  to  extreme  old 
age.  The  ectodermic  and  mesodermic  curves  during  this 
portion  of  the  life  span  are  nearly  parallel,  diverging 
only  slightly  from  each  other  with  advancing  age.  The 
curve  for  the  death  rate  resulting  from  breakdown  of 
organs  of  endodermic  origin  has  an  entirely  different 
course.  It  rises  sharply  for  ten  years  after  the  low  point 
in  early  youth,  and  then  makes  a  rather  sharp  bend  at 
about  age  22,  and  passes  off  to  the  end  of  the  life  span, 
at  a  reduced  rate  of  change.  In  consequence  of  this  it 
crosses  the  mesodermic  line  at  age  60.  From  that  point 
on  to  the  end  of  life  deaths  from  breakdo^vn  of  organs 
of  mesodermic  origin  stand  first  in  importance. 

Figure  40  shows  the  same  set  of  facts  for  the  female, 
and  at  once  a  number  of  strildng  differences  between  the 
conditions  in  the  two  sexes  appear.  In  the  first  place, 
the  breakdo^vn  of  mesodermic  organs  is  practically  of 
equal  importance  in  determining  the  mortality  of  infants 
with  the  breakdowai  of  endodermic  organs,  in  the  case  of 
the  female.  Tliis  fact,  of  course,  arises  because  of  the 
heavy  mortality  of  infancy  due  to  failure  of  the  female 
reproductive  organs,  a  matter  wliich  has  already  been 
discussed.  The  curve  for  breakdown  of  the  ectodermic 
organs  follows  substantially  the  same  kind  of  course  in 
the  female  as  it  does  in  the  male.  The  mesoderm  and 
endoderm  lines  cross  nearly  20  years  earlier  in  the  case 
of  females  than  in  the  males.  This  circumstance  arises 
from  the  fact  that  throughout  life  the  mesodermic  organs 
play  a  relatively  more  important  role  in  the  determina- 
tion of  mortalitv  in  the  female  than  they  do  in  the  male. 

What  reward  in  the  way  of  useful  generalization  may 

10 


146 


BIOLOGY  OF  DEATH 


be  claimed  from  the  details  reviewed  in  this  and  the  pre- 
ceding chapter?  I  hope  that  these  facts  will  have  served 
in  some  measure  to  complete  and  round  out  in  clearer 


lOOOc: 


AGE 
Fig.  40. — Showiog  specific  death  rates  for  females,  classified  in  the  same  manner  as  in  Fig.  39. 

outlines  one  part  of  the  picture  of  the  general  biology  of 
death.  It  has  been  shown  in  what  has  preceded  that  nat- 
ural death  is  not  a  necessarv  or  inherent  attribute  or 


EMBRYOLOGY  AND  HUMAN  MORTALITY  147 

consequence  of  life.  Many  cells  are  potentially  immor- 
tal and  the  potentiality  is  actually  realized  if  appropriate 
conditions  are  provided.  Protozoa  are  immortal,  (ierm 
cells  are  immortal.  Various  somatic  cells,  and  even  tis- 
sues have  been  proved  to  be  potentially  immortal  by 
demonstrating  in  a  variety  of  ways  that  under  appro- 
priate conditions  they  continue  to  live  indefinitely.  This 
is  the  lesson  taught  us  on  the  one  hand  by  successive 
transplantations  of  tumor  cells,  which  are  only  modified 
somatic  cells,  and  on  the  other  hand  by  successful  cul- 
ture of  many  sorts  of  somatic  cells  in  vitro. 

Analytical  consideration  of  the  matter  shows  very 
clearly  that  the  somata  of  multicellular  organisms 
die  because  of  the  differentiations  and  specializations 
of  structure  and  function  which  they  exhibit  in  their 
make-up.  Certain  cells  are  differentiated  to  carry  on 
certain  specialized  functions.  In  this  specialization  they 
forego  their  power  of  independent  and  indefinitely  con- 
tinued existence.  The  cells  lining  the  lungs,  for  example, 
must  depend  in  the  body  upon  the  unfailing  normal  ac- 
tivity of  the  cells  of  the  alimentary  tract  and  the  blood  in 
order  that  they,  the  epithelial  cells  of  the  hmgs,  may  get 
proper  nutrition.  If  in  such  an  interlocking  and  mu- 
tually dependent  system  any  one  part  through  ac<^ident 
or  in  any  way  whatever  gets  deviated  from  its  normal 
functioning,  the  balance  of  the  whole  system  is  upset.  If 
the  departure  of  any  part  from  its  normal  functional 
course  is  great  enough  to  be  beyond  correction  promptly 
through  the  normal  regulatory  powers  of  the  organism, 
death  of  the  whole  ^\dll  surely  ensue. 

What  I  have  tried  to  show  in  this  and  the  ]n-ecoding 
chapter  is  a  quantitative  picture  of  how  the  different 
organ  systems  get  out  of  balance,  and  wreck  the  whole 


148  BIOLOGY  OF  DEATH 

machine.  The  broad  orderliness  and  lawfulness  of  the 
whole  business  of  human  mortality  is  impressive.  We 
have  seen  that  different  organ  systems  have  well-defined 
times  of  breakdo^vn.  Or,  put  in  another  way,  we  see  that 
in  the  human  organism,  just  as  in  the  automobile,  the 
serviceability  of  the  different  parts  varies  greatly.  The 
heart  outwears  the  lungs,  the  brain  outwears  both.  But 
we  have  further,  I  believe,  got  an  inlding  of  the  funda- 
mental reason  why  these  things  are  so.  It  is  broadly 
speaking,  because  evolution  is  a  purely  mechanistic  pro- 
cess instead  of  being  an  intelligent  one.  All  the  parts  are 
not  perfected  by  evolution  to  even  an  approximately  equal 
degree.  It  is  conceivable  that  an  omnipotent  person 
could  have  made  a  much  better  machine,  as  a  whole,  than 
the  human  body  which  evolution  has  produced,  assuming, 
of  course,  that  he  had  first  learned  the  trick  of  making 
self-regulating  and  self-reproducing  machines,  such  as 
living  machines  are.  He  would  presumably  have  made  an 
endoderm  with  as  good  resisting  and  wearing  qualities 
as  the  mesoderm  or  ectoderm.  Evolution  by  the  hap- 
hazard process  of  trial  and  error  which  we  call  natural 
selection,  makes  each  part  only  just  good  enough  to  get 
by.  In  the  very  nature  of  the  process  itself  it  cannot 
possibly  do  anything  any  more  constructive  than  this. 
The  workmanship  of  evolution,  from  a  mechanical 
point  of  view,  is  extraordinarily  like  that  of  the  average 
automobile  repair  man.  If  evolution  happens  to  be  fur- 
nished by  variation  with  fine  materials,  as  in  the  case 
of  the  nervous  system,  it  has  no  objection  to  using  them, 
but  it  is  equally  ready  to  use  the  shoddiest  of  endoderm 
provided  it  mil  hold  together  just  long  enough  to  get 
the  machine  by  the  reproductive  period. 

It  furthermore  seems  to  me  that  the  results  presented 


EMBRYOLOGY  AND  HUMAN  MORTALITY  149 

in  this  chapter  add  one  more  link  to  the  already  strong 
chain  of  evidence  which  indicates  the  higlily  important 
part  played  by  innate  constitntional  ])i()lo<z:ical  factors 
as  contrasted  with  environmental  factors  in  the  deter- 
mination of  the  observed  rates  of  human  mortality.  Here 
we  have  grouped  human  mortality  into  broad  classes 
wliicli  rest  upon  a  strictly  biological  basis.  Wlu'ii  this 
is  done  it  is  found  that  the  proportionate  su])division  of 
the  mortality  among  the  several  causes — in  sliort  the 
death  ratios  in  the  sense  of  Fisher — is  strikingly  similar 
in  such  widely  dissimilar  environments  as  the  United 
States,  England  and  Southern  Brazil. 


CHAPTER  VI 

THE  INHERITANCE  OF  DURATION  OF 

LIFE  IN  MAN 

We  have  seen  that  in  the  case  of  man,  where  alone 
quantitative  data  are  available,  the  breakdown  of  partic- 
ular organ  systems,  and  consequent  death  of  the  whole, 
occurs  in  a  highly  orderly  manner  in  respect  of  time  or 
age.  Each  organ  system  has  a  characteristic  time  curve 
for  its  breakdowm,  differing  from  the  curve  of  any  other 
system.  The  problem  which  now  confronts  us  is  to  find 
out  what  lies  back  of  these  characteristic  time  curves  and 
determines  their  form.  In  view  of  the  biological  facts 
about  death  which  we  have  learned,  what  determines  that 
John  Smith  shall  die  at  58,  while  Henry  Jones  lives  to 
the  obviously  more  respectable  age  of  85?  We  have 
seen  that  there  is  every  reason  to  believe  that  all  the 
essential  cells  of  both  their  bodies  are  inherently  capable 
under  proper  conditions  of  li\dng  indefinitely.  It  fur- 
ther appears  probable  that  it  is  the  differentiated  and 
specialized  structure  of  their  bodies  which  prevents  the 
realization  of  these  favorable  conditions.  But  all  this 
helps  us  not  at  all  to  understand  why  in  fact  one  lives 
nearly  30  years  longer  than  the  other. 

It  may  help  to  visualize  this  problem  of  the  determina- 
tion of  longevity  to  consider  an  illustrative  analogy. 
Men  behave  in  respect  of  their  duration  of  life  not  unlike 
a  lot  of  eight-day  clocks  cared  for  by  an  unsystematic 
person,  who  does  not  wind  them  all  to  an  equal  degree 
and  is  not  careful  about  guarding  them  from  accident. 
Some  he  winds  up  fully,  and  they  run  their  full  eight  days. 

150 


THE  INHERITANCE  OF  DURATION  151 

Others  he  winds  only  halfway,  and  they  stoi)  after  four 
days.   Again  the  clock  which  has  been  wound  up  for  the 
full  eight  days  may  fall  off  the  shelf  and  bo  ])rc)u^dit  to  a 
stop  at  the  third  day.     Or  someone  may  throw  some  sand 
in  the  works  when  the  caretaker  is  off  his  guard.     So, 
similarly,  some  men  behave   as  thonpfh   thev  had  boon 
wound  up  for  a  full  90-year  run,  while  others  are  but 
partially  w^ound  up  and  stop  at  40  or  65,  or  some  other 
point.     Or,  again,  the  man  wound  up  for  80  years  may, 
like  the  clock,  be  brought  up  much  short  of  that  by  an 
accidental  invasion  of  microbes,  playing  the  role  of  the 
sand  in  the  w^orks  of  the  clock.     It  is  of  no  avail  for 
either  the  clock  or  the  man  to  say  that  the  elements  of  the 
mechanism  are  in  w^hole  or  in  major  part  capable  of  fur- 
ther ser\ace.     The  essential  problem  is :  what  determines 
the  goodness  of  the  original  winding?     And  what  rela- 
tive part  do  external  things  play  in  bringing  the  running 
to  an  end  before  the  time  wdiich  the  original  \vinding  w\as 
good  for?     It  is  with  this  problem  of  the  w^inding  up  and 
running  of  the  human  mechanism  that  the  present  chap- 
ter will  deal. 

There  are  tw^o  general  classes  of  factors  which  may 
be  involved  here.  These  are,  on  the  one  hand,  heredity 
and,  on  the  other  hand,  environment,  using  the  latter  term 
in  the  broadest  sense.  Inasmuch  as  we  can  be  reason- 
ably sure  on  a  'priori  grounds  that  longevity,  like  most 
other  biological  phenomena,  is  influenced  by  both  hered- 
ity and  environment  the  problem  practically  reduces  itself 
to  the  measuring  of  the  relative  importance  of  each  of 
these  two  factor  groups  in  determining  the  results  we  see. 
But  before  we  start  the  discussion  of  exact  measurements 
in  this  field  let  us  first  examine  some  of  the  general  evi- 


152  BIOLOGY  OF  DEATH 

dence  that  heredity  plays  any  part  at  all  in  the  deter- 
mination of  longevity. 

THE  HYDE  FAMILY 

The  first  material  which  we  shall  discuss  is  that  pro- 
vided by  the  distinguished  eugenist,  Dr.  Alexander 
Graham  Bell,  in  his  study  of  the  Hyde  family.  Every 
genealogist  is  familiar  with,  the  ''Genealogy  of  the  Hyde 
Family,"  by  Eeuben  H.  Walworth.  It  is  one  of  the  fin- 
est examples  in  existence  of  careful  and  painstaking 
genealogical  research.  Upon  the  data  included  in  this 
book,  Bell  has  made  a  most  interesting  and  penetrating 
analysis  of  the  factors  influencing  longevity.  At  first 
thought  one  might  conclude  that  liighly  biased  results 
would  probably  flow  from  the  consideration  of  only  one 
family.  Bell  meets  this  point  very  well,  however,  in  the 
following  words : 

A  little  consideration  will  show  that  the  descendants  did  not  constitute 
a  single  family  at  all,  and  indeed  had  very  little  of  the  Hyde  blood  in  them. 

Even  the  children  of  William  Hyde  owed  only  half  of  their  blood  to 
him,  and  one-half  to  his  wife.  The  grandchildren  owed  only  one-quarter  of 
their  blood  to  William  Hyde,  and  three-quarters  to  other  people,  etc.  The 
descendants  of  the  seventh  generation,  and  there  are  hundreds  of  them,  owed 
only  one  sixty-fourth  of  their  blood  to  William  Hyde,  and  sixty-three 
sixty-fourths  to  the  new  blood  introduced  through  successive  generations  of 
marriages  with  persons  not  of  the  Hyde  blood  at  all. 

It  will  thus  be  seen  that  the  thousands  of  descendants  noted  in  the 
Hyde  Genealogy  constitute  rather  a  sample  of  the  general  population  of 
the  country  than  a  sample  of  a  particular  family  in  which  family  traits 
might  be  expected  to  make  their  appearance. 

The  substantial  normality  of  the  material  is  shown 
in  Figure  41,  wliich  gives  the  l^  line,  that  is,  the  number 
of  survivors  at  each  age,  of  the  1,606  males  and  1,352 
females  for  whom  data  were  available.  The  solid  line 
is  the  male  l^,  line  and  the  dotted  line  the  female  l^  -  It 
is  at  once  apparent  that  the  curves  have  the  same  general 


THE  INHERITANCE  OF  DURATION 


153 


sweep  in  their  passage  over  the  span  of  life  as  has  the 
general  population  life  curve  discussed  in  the  preceding 
chapter.  The  descent  is  a  little  steeper  in  early  adult 
life.  The  female  curve  differs  in  two  respects  from  the 
normal  general  population  curves.     In  the  first  place. 


B 


10      15     ZO     25     30     35    40    45     50     55    CO     Cs5     "O     "5 

AOL 
Fio.  41. — Showing  survival  curves  of  members  of  the  Hyde  family  (Plotted  from  Bell's  data). 

beginning  at  age  15  and  continuing  to  age  90,  the  female 
curve  lies  below  that  for  the  males,  whereas  nonnally  for 
the  general  population  it  lies  above  it.  This  denotes  a 
shorter  average  duration  of  life  in  the  females  than  in 
the  males,  the  actual  figures  being  35.8  years  for  tlie  males 
and  33.4  years  for  the  females.  Bell  attributes  the  dif- 
ference to  the  strain  of  child-bearing  by  the  females  in 


154  BIOLOGY  OF  DEATH 

this  rather  highly  fertile  group  of  people,  belonging  in 
the  main  to  a  period  when  restrictions  upon  size  of  family 
were  less  common  and  less  extensive  than  now.  In  the 
second  place,  the  female  l^  curve  is  actually  convex  to 
the  base  throughout  a  considerable  portion  of  middle 
life  whereas,  normally,  this  portion  of  the  curve  presents 
a  concave  face  to  the  base. 

Apart  from  these  deviations,  which  are  of  no  partic- 
ular significance  for  the  use  which  Bell  makes  of  the 
data,  the  Hyde  material  is  essentially  normal  and  simi- 
lar to  what  one  would  expect  to  find  in  a  random  sample 
of  the  general  population.  In  this  material  there  were 
2,287  cases  in  which  the  ages  at  death  of  the  persons  and 
the  ages  at  death  of  their  fathers  were  knowm.  It  occurred 
to  Bell  to  arrange  this  material  in  such  a  way  as  to 
show  what,  if  any,  relation  existed  between  age  at  death 
of  the  parent  and  that  of  the  offspring.  He  arranged 
the  parents  into  four  groups,  according  to  the  age  at  which 
they  died,  and  the  offspring  into  five  groups  upon  the 
same  basis.  In  the  case  of  the  parents  the  groups  were : 
First,  those  dying  under  40 ;  second,  between  40  and  60 ; 
third,  between  60  and  80 ;  and  fourth,  at  age  80  and  over. 
The  groups  for  the  offspring  were  the  same,  except  that 
the  first  was  divided  into  two  parts,  namely,  those  dying 
under  20  and  those  dying  between  20  and  40.  The  result- 
ing figures  are  exhibited  in  Table  14. 

The  results  for  father  and  offspring  are  sho\vn  in 
Figure  42,  based  upon  the  data  of  Table  14.  In  each 
of  the  5  polygons,  one  for  each  offspring  group,  the  first 
dot  shows  the  percentage  of  fathers  dying  under  40; 
the  second  dot  the  percentage  of  fathers  dying  between 
40  and  60 ;  and  so  on,  the  last  dot  in  each  curve  shomng 
the  percentage  of  fathers  dying  at  age  80  and  over.     It 


THE  INHERITANCE  OF  DURATION 


1 55 


TABLE  14 

Analysis  of  the  Hyde  family  data  by  person's  age  at  death,  shounng  the  number 

and  percentage  having  (a)  fathers  and  (6)  mothrrs  who  died 

at  the  age  periods  named.     (From  Bell) 


Person's  age  at  death 

Father* 

8  age  at  death 

Stated 

-40 

40-60 

60-80 

hO-h 

Stated 

2,287 

669 
538 
467 
428 
185 

66 
20 

18 

12 

13 

3 

522 

189 

140 

116 

57 

20 

1,056 

299 
2ti9 
215 
196 

i  i 

643 

Under  20 

161 

20  and  under  40 

111 

40  and  under  60 

124 

60  and  under  80 

162 

80  and  over 

85 

Percentages 


Stated 

100.0 

100.0 
100.0 
100.0 
100.0 
100.0 

2.9 

3.0 
3.4 
2.6 
3.0 
1.6 

22.8 

28.2 
26.0 
24.8 
13.3 
10.8 

46.2 

44.7 
50.0 
46.0 
45.8 
41.6 

28.1 

Under  20 

24.1 

20  and  under  40 

20.6 

40  and  under  60 

26.6 

60  and  under  80 

37.5 

80  and  over 

46.0 

PersoD's  age  at  death 

Mother 

'b  age  at  death 

Stated 

-40 

40-60 

60-80 

80  + 

Stated 

1,805 

511 
407 
379 
360 
148 

191 

88 
42 
27 
26 
8 

435 

129 

104 

92 

80 

30 

713 

199 
176 
159 
129 
50 

466 

Under  20 

95 

20  and  under  40 

85 

40  and  under  60 

101 

60  and  under  80 

125 

80  and  over  ...                         

60 

Stated 


Under  20 

20  and  under  40 
40  and  under  60 
60  and  under  80 
80  and  over  .  .  .  . 


Percentages 


100.0       10.6      24.1       39.5      25.8 


100.0 

17.2 

25.2 

39.0 

18.6 

100.0 

10.3 

25.6 

43.2 

20.9 

100.0 

7.1 

24.3 

42.0 

26.6 

100.0 

7.2 

22.2 

35.9 

34.7 

100.0 

5.4 

20.3 

33.8 

40.5 

156 


BIOLOGY  OF  DEATH 


is  to  these  last  dots  that  attention  should  be  particularly 
directed.  It  will  be  noted  that  the  dotted  line  connecting 
the  last  dots  of  each  of  the  5  polygons  in  general  rises 
as  we  pass  from  the  left-hand  side  of  the  diagram  to  the 
right-hand  side.  In  the  case  of  offspring  dying  under  20, 
24  per  cent,  of  their  fathers  died  at  ages  over  80.    About 


660 

53d 

A  67 

42a 

I&5 

PERSONS 

PERSONS 

PERSONS 

PERSONS 

PERSONS 

DIED 

DIED 

DIED 

DIED 

DIED 

-20 

ZO-  AC 

40-60 

to-eo 

60t 

SO 


AO 


30 


20 


10 


50 


AO 


30 


zo 


lO 


~      AO      60      60       -      ao      60      60       -       AO      60     60      -       AO      60      80       -       AO      60      60 
AO     to      60       +      40      60      60       +      AO6O6O+4O60      80-h       AO     60     80       + 

Fig.  42. — Influence  of  father's  age  at  death  upon  longevity  of  offspring.  First  dot  in 
each  diagram  shows  the  percentage  having  fathers  who  died  at  40;  second  dot  the  percent- 
age having  fathers  who  aied  from  40-60;  third  dot  the  percentage  having  fathers  who  died 
from  60-80;  fourth  dot  the  percentage  having  fathers  who  died  80-|-  (After  Bell). 

21  per  cent,  of  the  fathers  of  offspring  dying  between  20 
and  40  lived  to  be  80  years  or  over.  For  the  next  longer- 
lived  group  of  offspring,  dying  between  40  and  60,  the 
percentage  of  fathers  living  to  80  or  over  rose  to  27  per 
cent.  In  the  next  liigher  group,  the  percentage  is  nearly 
38,  and  finally  the  extremely  long-lived  group  of  offspring, 
the  185  persons  who  died  at  ages  of  80  and  over,  had  46 
per  cent,  or  nearly  one-half  of  their  fathers  living  to  the 
same  great  age.  In  other  words,  we  see  in  general  that 
the  longer-lived  a  group  of  offspring  is,  on  the  average, 
the  longer-lived  are  their  fathers,  on  the  average;  or, 
put  in  another  way,  the  higher  the  percentage  of  very 


THE  INHERITANCE  OF  DURATION         157 

long-lived  fathers  which  this  group  will  have  as  com- 
pared with  shorter-lived  individuals. 

Figure  43  shows  the  same  sort  of  data  for  mothers 
and  offspring.  Here  we  see  the  curve  of  great  longevity 
of  parents  rising  in  an  even  more  marked  manner  than 
was  the  case  with  fathers  of  oifspring.     The  group  of 


so 


Sll 

407 

379 

360 

I4S 

PLRSONS 

PCPSONS 

PCf?SONS 

PcesoNS 

P€tfS0N8 

DIED 

DiCD 

DICD 

DILD 

OCD 

-20 

20-4C 

40 -60 

60-60 

604. 

SO 


40 


30 


20 


10 


40 


30 


20 


40      60     SO       -       40      60      80       -       ao      60     80       -       ^C      60      &0      -       40      60      BO 
40      60       80       ■*■       4-0      60      60       +       40      60      80       +       40      60      60       ■*■      40      60      60       + 


Fig.  43. — Influence  of  mother's  age  at  death  upon  longevity  of  offspring.  First  dot  in 
each  diagrarn  shows  the  percentage  having  mothers  who  died  at  40;  second  dot  the  per- 
centage having  mothers  who  died  at  40-60;  third  dot  the  percentage  ha\Tng  mothers  who 
died  60-80;  fourth  dot  the  percentage  having  mothers  who  died  80+  (After  Bell). 

offspring  dying  at  ages  under  20  had  only  19  per  cent, 
of  their  mothers  living  to  80  and  over,  whereas  the 
group  of  offspring  who  lived  to  80  and  beyond  had  41 
per  cent,  of  their  mothers  attaining  the  same  gi'eat  age. 
At  the  same  time  we  note  from  the  dotted  line  at  the  bot- 
tom of  the  chart  that  as  the  average  age  at  death  of  the 
offspring  increases,  the  percentage  of  mothers  dying  at 
early  ages,  namely,  under  40,  as  given  by  the  first  dots, 
steadily  decreases  from  17  per  cent,  at  the  first  group  to 
just  over  5  per  cent,  for  the  offspring  dying  at  very 
advanced  ages. 


158 


BIOLOGY  OF  DEATH 


These  striking  results  demonstrate  at  once  that  there 
is  a  definite  and  close  connection  between  the  average 
longevity  of  parents  and  that  of  their  children.  Ex- 
tremely long-lived  children  have  a  much  higher  percent- 
age of  extremely  long-lived  parents  than  do  shorter  lived 
children.  While  the  diagrams  demonstrate  the  fact  of 
this  connection,  they  do  not  measure  its  intensity  with 
as  great  precision  as  can  be  obtained  by  other  methods 
of  dealing  with  the  data.  A  little  farther  on  we  shall 
take  up  the  consideration  of  this  more  precise  method 
of  measurement  of  the  hereditary  influence  in  respect 
of  longe\T.ty. 

In  the  preceding  diagrams  we  have  considered  each 
parent  separately  in  connection  with  the   offspring  in 

TABLE  15 

Longevittj  of  -parents  of  persons  dying  at  80  and  over.     (From  Bell) 


Age  at  death  of  parents 

Number  of 
persons 

Number  of 

persons  lived 

80  + 

Per  cent,  of 

persons  lived 

80  + 

Stated 

1,594 

827 
583 
184 

337 
246 

139 

44 
57 
38 

38 
19 

8.7 

Lived  to  be  804- 
Neither  oarent 

5.3 

One  parent  (not  other) 

Both  parents 

9.8 
20.6 

Father  (not  mother) 

Mother  (not  father) 

11.3 

7.7 

regard  to  longevity.  We  shall,  of  course,  get  precisely 
the  same  kind  of  result  if  we  consider  both  parents  to- 
gether. For  the  sake  of  simplicity,  taking  only  the  cases 
of  extreme  longevity,  namely,  persons  living  to  80  or 
over — the  essential  data  are  given  in  Table  15. 

From  tliis  table  it  is  seen  that  where  neither  parent 
lived  to  be  80,  only  5-3  per  cent,  of  the  offspring  lived  to 
be  80  or  over,  the  percentage  being  based  upon  827 


THE  INHERITANCE  OF  DURATION         159 

cases.     Where  one  parent,  but  not  the  other,  livfd  to  be 
80  or  older,  9.8  per  cent,  of  the  otTspring  lived  to  l)o  80 
or  older,  the  percentage  here  being  based  upon  583  cases. 
Where  both  parents  lived  to  be  80  or  older  20. G  per  cent,  of 
the  persons  lived  to  the  same  great  age,  the  percentage  be- 
ing based  upon  184  cases.    Thus  it  appears  that  in  this 
group  of  people  four  times  as  many  attained  great  longev- 
ity if  both  their  parents  lived  to  an  advanced  age,  as 
attained  tliis  age  when  neither  parent  exhibited  great 
longevity.     The  figures  from  the  Hyde  family  seem  fur- 
ther to  indicate  that  the  tendency  of  longevity  is  inherited 
more    strongly   through   the   father   than   through   tlu* 
mother.     Where  the  father,  but  not  the  mother.  Lived  to 
be  80  or  older,  11.3  per  cent,  of  the  persons  lived  to  age 
80  or  more,  there  being  337  cases  of  this  kind.     Where 
the  mother,  but  not  the  father  lived  to  be  80  or  older, 
only  7.7  per  cent.,  or  nearly  4  per  cent,  fewer  of  the 
persons  lived  to  the  advanced  age  of  80  or  more,  there 
being  246  cases  of  this  sort.     Too  much  stress  is  not, 
however,  to  be  laid  upon  this  parental  difference  because 
the  samples  after  all  are  quite  small. 

One  other  point  in  this  table  deserves  consideration. 
Out  of  the  1,594  cases  as  a  whole,  less  than  9  per  cent, 
of  the  persons  lived  to  the  advanced  age  of  80  or  more. 
But  out  of  this  number  there  are  767,  or  48.1  per  cent., 
nearly  one-half  of  the  whole,  who  had  parents  who  lived 
to  80  or  more  years. 

Another  interesting  and  significant  way  in  which  one 
may  see  the  great  influence  of  the  age  of  the  parents  at 
death  upon  the  longevity  of  the  offspring,  is  indicateil 
in  Table  16,  where  we  have  the  average  duration  of 
life  of  individuals  whose  fathers  and  mothers  died  at 
the  speciiied  ages. 


160 


BIOLOGY  OF  DEATH 


We  see  that  the  longest  average  duration  of  life,  or 
expectation  of  life,  was  of  that  group  which  had  both 
mothers  and  fathers  living  to  age  80  and  over.  The 
average  duration  of  life  of  these  persons  was  52.7  years. 
Contrast  this  with  the  average  duration  of  life  of  those 
whose  parents  both  died  under  60  years  of  age,  where 

TABLE  16 

Showing  the  influence  of  a  considerable  degree  of  longevity  in    both  father 

and  mother  upon  the  expectation  of  life  of  the  offspring.     {After  Bell). 

{In  each  cell  of  the  table  the  open  figure  is  the  average  duration  of 

life  of  the  offspring  and  the  bracketed  figure  is  the  number  of 

cases  upon  which  the  average  is  based). 


Father's  age 
at  death 

Mother's  age  at  death 

Under  60 

60-80 

Over  80 

Under  60 

32.8  years 
(128) 

33 . 4  years 
(120) 

36 . 3  years 
(74) 

60-80 

35.8 
(251) 

38.0 
(328) 

45.0 
(172) 

Over  80 

42.3 
(131) 

45.5 
(206) 

52.7 
(184) 

the  figTire  is  32.8  years.  In  other  words,  it  added  al- 
most exactly  20  years  to  the  average  life  of  the  first 
group  of  people  to  have  extremely  long-lived  parents, 
instead  of  parents  dying  under  age  60.  In  each  column 
of  the  table  the  average  duration  of  life  advances  as  we 
proceed  from  top  to  bottom — that  is,  as  the  father's  age 
at  death  increases — and  in  each  row  of  the  table  the  aver- 
age expectation  of  life  of  the  offspring  increases  as  we 
pass  from  left  to  right — that  is,  with  increasing  age  of 
the  mother  at  death.  However  the  matter  is  taken,  a 
careful  selection  of  one's  parents  in  respect  of  longevity 
is  the  most  reliable  form  of  personal  life  insurance. 


THE  INHERITANCE  OF  DURATION  ic.l 

How  great  and  deep  is  the  significance  oi'  tiie  facts 
shown  in  Table  16  may  best  be  brought  home  to  the  mind 
by  means  of  a  comparison.  Suppose  tliis  (question  to 
be  asked:  by  how  great  an  amount  would  the  average 
expectation  of  life  at  birth  (which  in  a  stable  population 
is  the  same  thing  as  the  mean  duration  of  Ufe)  be  increased 
if  all  the  reasonably  preventable  deaths  were  prevented? 
If,  say  75  per  cent,  of  all  the  deaths  from  pulmonary  tuber- 
culosis did  not  occur;  if  40  per  cent,  of  the  deaths  from 
Bright 's  disease  were  prevented;  and,  in  general,  il" 
all  that  medicine  and  hygiene  knows  today  were  put 
into  reasonably  effective  operation,  and  nobody  died 
except  when  and  from  such  causes  as  could  in  no 
way  be  influenced  by  what  medical  science,  good  envi- 
ronment, etc.,  have  to  offer:  by  how  much  then  would 
the  expectation  of  life  be  greater  than  it  now  is?  We 
have  seen  that  to  have  one^s  parents  live  to  80  or  over 
increases  the  expectation  of  life  20  years,  as  compared 
with  that  of  persons  whose  parents  die  under  60  years  of 
age.  By  how  much  more  would  the  expectation  of  life 
be  extended  if  all  reasonably  preventable  deaths  were 
prevented? 

A  thorough  and  critical  answer  to  this  question  is 
afforded  by  an  investigation  of  Forsyth's,  conducted 
along  the  most  exact  and  approved  actuarial  lines. 
Some  years  ago,  Professor  Irving  Fisher  sent  a  list  of 
some  90  diseases  to  a  group  of  the  most  prominent  medi- 
cal authorities  in  this  country,  and  asked  them  to  desig- 
nate what  percentage  of  the  deaths  due  to  each  disease 
they  considered  preventable.  The  results  of  this  incpiiry 
were  tabulated  in  an  extremely  conservative  manner, 
with  the  result  set  forth  in  Table  16a,  wliieli  is  copied 

from  Forsyth's  paper  (pp.  762-763). 
11 


162 


BIOLOGY  OF  DEATH 


TABLE  16  a 

Showing  Fisher's  ratios  of  preventability  for  the  diseases  enumerated  in  the 

mortality  statistics  of  the   United  States,    together  with    the    relative 

importance  of  each  disease  as  indicated  by  the  percentage  the 

number  of  its  deaths  bears  to  the  total  number  of  deaths 


1 
2 
3 

4 
5 
6 
7 
8 
9 
10 
11 
12 
13 
14 
15 
16 
17 
18 
19 
20 
21 
22 
23 
24 
25 
26 
27 
28 
29 
30 
31 
32 
33 
34 
35 
36 


37 
38 
39 
40 
41 
42 


Causes  of  death 


Premature  birth 

Congenital  malformation  of  the  heart 

Other  congenital  malformations 

Congenital  debility 

Hydrocephalus 

Venereal  diseases 

Diarrhoea  and  enteritis 

Measles 

Acute  bronchitis 

Bronchopneumonia 

Whooping  cough 

Croup  

Meningitis 

Diseases  of  larynx — not  laryngitis 

Laryngitis 

Diphtheria 

Scarlet  fever 

Diseases  of  lymphatics 

Tonsillitis 

Tetanus   

Tuberculosis — not  of  lungs 

Abscess 

Appendicitis 

Typhoid  fever 

Puerperal  convulsions   

Puerperal  septicaemia 

Other  diseases  of  childbirth 

Diseases  of  tubes 

Peritonitis 

Smallpox 

Tuberculosis  of  lungs 

Violence 

Malarial  fever 

Septicaemia 

Epilepsy 

General,  ill-defined,  and  unknown  causes  (in 
eluding  "heart  failure,"  *'dropsy,"  and  "con 
vulsions") 

Erysipelas 

Pneumonia  (lobar  and  unqualified) 

Acute  nephritis 

Pleurisy 

Acute  yellow  atrophy  of  liver 

Obstructions  of  intestines 


Prominence  of 

disease.  Percent. 

of  all  deaths 

Ratio  of 

preventability. 

Per  cent. 

2.0 

40 

.55 

0 

.3 

0 

2.3 

40 

.1 

0 

.3 

70 

7.74 

60 

.8 

40 

1.1 

30 

2.4 

50 

.9 

40 

.3 

75 

1.6 

70 

.07 

40 

.06 

40 

1.4 

70 

.5 

50 

.01 

20 

.05 

45 

.19 

80 

.17 

75 

.08 

60 

.7 

50 

2.0 

85 

.2 

30 

.4 

85 

.36 

50 

.1 

65 

.5 

55 

.01 

75 

9.9 

75 

7.5 

35 

.2 

80 

.3 

40 

.29 

0 

9.2 

30 

.3 

60 

7.0 

45 

.6 

30 

.27 

55 

.02 

0 

.6 

25 

I 


THE  INHERITANCE  OF  DURATION 


163 


TABLE  IG a— Continued 


Causes  of  death 


4.}    Alcoholism 

44  Hemorrhage  of  lungs 

45  Diseases  of  the  thyroid  body.  .  . 

46  Ovarian  tumor 

47  Uterine  tumor 

48  Rheumatism   

49  Gangrene  of  lungs 

50  Anaemia,  leukaemia 

51  Chronic  poisonings 

52  Congestion  of  lungs 

53  Ulcer  of  stomach 

54  Carbuncle 

55  Pericarditis 

56  Cancer  of  female  genital  organs 

57  Dysentery 

58  Gastritis 

59  Cholera  nostras 

60  Cirrhosis  of  liver 

61  General  paralysis  of  insane 

62  Hyatid  tumors  of  liver 

63  Endocarditis 

64  Locomotor  ataxia 

65  Diseases  of  veins 

66  Cancer  of  breast 

67  Diabetes 

68  Biliary  calculi 

69  Hernia   

70  Cancer  not  specified 

71  Tumor 

72  Bright's  disease 

73  Embolism  and  thrombosis 

74  Cancer  of  intestines 

75  Cancer  of  stomach  and  liver. . .  . 

76  Calculi  of  urinary  tract 

77  Cancer  of  mouth 

78  Heart  disease 

79  Influenza 

80  Asthma  and  emphysema 

81  Angina  pectoris 

82  Apoplexy 

83  Cancer  of  skin 

84  Chronic  bronchitis 

85  Paralysis 

86  Softening  of  brain 

87  Diseases  of  arteries 

88  Diseases  of  bladder 

89  Gangrene 

90  Old  age 


Prominence  of 

diseaBC.  Percent. 

uf  all  deaths 


1 


.4 
.1 
.02 
.07 
.1 
.5 
.03 
.4 
.05 
.4 
.2 
.03 
.1 
.6 
.5 
.65 
.09 
.9 
.3 

.002 
.8 
.17 
.04 
.4 
.8 
.17 
.27 
.9 
.08 
i.6 
.26 
.55 
.7 
.03 
.1 
.1 
.7 
.23 
.4 
.4 
.2 
.8 
.0 
.2 
.83 
.2 
.25 
0 


lUtio  of 

preventability. 

Per  cent. 


85 
80 
10 

0 
60 
10 

0 
50 
70 
50 
50 
50 
10 

0 
80 
50 
50 
60 
75 
75 
25 
35 
40 

0 
10 
40 
70 

0 

0 
40 

0 

0 

0 
10 

0 
25 
50 
30 
25 
35 

0 
30 
50 

0 
10 
45 
60 

0 


164 


BIOLOGY  OF  DEATH 


It  will  be  seen  that  these  ratios  of  preventability  are 
not  all  100  per  cent.  They  are  not  the  wild  overstate- 
ments of  the  propagandist.  But  they  do  represent,  if 
they  could  be  realized,  substantial  reductions  from  exist- 
ing mortality  rates. 

TABLE  16  b 

Complete  expectations  of  life  as  based  upon  the  two  assumptions   that   deaths 
are  and  are  not  prevented  according  to  the  ratios  given  in  Table  16a 


Deaths 

Loss  in 

Age 

Deaths 

Loss  in 

Age 

Not  pre- 
vented 

Pre- 
vented 

Years 

Days 

Not  pre- 
vented 

Pre- 
vented 

Years 

Days 

0 

49.44 
56.03 
56.84 
56.64 
56.15 
55.51 
54.81 
54.06 
53.26 
52.43 
51.57 
50.69 
49.80 
48.91 
48.03 
47.15 
46.31 
45.50 
44.71 
43.93 
43.15 
42.37 
41.60 
40.83 
40.07 

62.11 
66.26 
66.28 
65.67 
64.94 
64.13 
63.27 
62.42 
61.54 
60.63 
59.72 
58.79 
57.86 
56.80 
56.00 
55.07 
54.16 
53.26 
52.36 
51.48 
50.59 
49.70 
48.82 
47.94 
47.06 

12 

10 

9 

9 

8 
8 
8 
8 
8 
8 
8 
8 
8 
7 
7 
7 
7 
7 
7 
7 
7 
7 
7 
7 
6 

245 

84 

161 

11 

288 

226 

168 

131 

102 

73 

55 

37 

22 

321 

354 

336 

310 

277 

237 

201 

161 

120 

80 

40 

261 

25 

39.31 
38.56 
37.82 
37.08 
36.34 
35.61 
34.88 
34.15 
33.42 
32.69 
31.96 
31.23 
30.50 
29.77 
29.03 
28.30 
27.57 
26.85 
26.12 
25.40 
24.68 
23.97 
23.26 
22.56 
21.87 

46.18 
45.31 
44.45 
43.58 
42.72 
41.86 
41.01 
40.15 
39.30 
38.46 
37.61 
36.76 
35.92 
35.08 
34.24 
33.40 
32.57 
31.74 
30.91 
30.09 
29.28 
28.47 
27.67 
26.87 
26.09 

6 

6 

6 

6 

6 

6 

6 

6 

5 

5 

5 

5' 

5 

5 

5 

^ 

o 
5 
4 
4 
4 
4 
4 
4 
4 
4 

318 

1 

26 

274 

2 

27 

230 

3 

28 

183 

4 

29 

139 

5 

30 

91 

6 

31 

47 

7 

32 

0 

8 

33 

321 

9 

34 

281 

10 

35 

237 

11 

36 

193 

12 

37 

153 

13 

38 

113 

14 

39 

77 

15 

40 

37 

16     

41 

0 

17 

42 

43 

325 

18 

288 

19 

44 

252 

20 

45 

46 

47 

48 

49 

219 

21 

183 

22 

150 

23 

113 

24 

80 

On  the  basis  of  the  mortality  experience  of  the  Regis- 
tration Area  for  11  years  (1900-1910)  Forsyth  calculated 
mortality  tables  on  the  assumption  that  the  ratios  of 
preventability  of  Table  16a  were  actually  in  full  opera- 
tion. The  results,  so  far  as  concerns  expectation  of  life, 
are  set  forth  in  Table  16b. 


THE  INHERITANCE  OF  DURATION 


IG") 


From  the  first  line  of  tliis  table  it  is  perceived  that 
the  total  increase  in  expectation  of  lif(*  which  would 
result  if  Fisher's  ratios  of  preventability  ^vere  fully 
realized  is  just  under  13  years!  How  unfavorably  this 
contrasts  wdth  the  20  years  increase  shown  by  the  two 

TABLE  16  b— Continued 


Deaths 

Loss  in 

Age 

Deaths 

LoMin 

Age 

Not  pre- 
vented 

Pre- 
vented 

Years 

Days 

Not  pre- 
vented 

Pre- 
vented 

Years 

Days 

50 

21.17 
20.47 
19.78 
19.09 
18.40 
17.74 
17.08 
16.45 
15.83 
15.23 
14.63 
14.05 
13.48 
12.92 
12.36 
11.82 
11.29 
10.77 
10.26 
9.77 
9.29 

25.30 
24.52 
23.74 
22.97 
,  22.21 
21.46 
20.72 
20.00 
19.30 
18.61 
17.93 
17.27 
16.61 
15.96 
15.32 
14.69 
14.07 
13.47 
12.87 
12.29 
11.71 

4 
4 
3 
3 
3 
3 
3 
3 
3 
3 
3 
3 
3 
3 
2 
2 
2 
2 
2 
2 
2 

47 
18 
350 
321 
296 
263 
234 
201 
193 
139 
110 
80 
47 
15 
350 
348 
285 
256 
223 
190 
153 

71 

8.82 
8.36 
7.93 
7.50 
7.09 
6.70 
6.31 
5.98 
5.64 
5.32 
5.02 
4.74 
4.47 
4.23 
4.01 
3.79 
3.58 
3.39 
3.22 
3.06 

11.15 
10.59 
10.04 
9.51 
8.99 
8.49 
8.00 
7.53 
7.07 
6.63 
6.20 
5.78 
5.38 
4.99 
4.62 
4.25 
3.89 
3.56 
3.27 
3.06 

2 
2 
2 
2 

1 

120 

51 

72 

84 

52. 

73 

40 

53 

74 

4 

54 

75 

329 

55. 

76 

288 

56.    .  . 

77 

252 

57 

78 

201 

58 

79 

157 

59 

80 

113 

60 

81 

66 

61 

82 

15 

62 

83 

332 

63 

84 

277 

64 

85 

223 

65 

86 

168 

66 

87 

113 

67 

88 

62 

68 

89 

18 

69 

90 

0 

70 

corner  diagonal  cells  of  Table  16!  No  more  striking 
demonstration  could  be  found  of  the  overw^helming  im- 
portance of  heredity  in  determining  duration  of  life.  For 
if  all  the  deaths  wliich  reason  will  justify  one  in  suppos- 
ing preventable  on  the  basis  of  what  is  now^  known,  were 
prevented  in  fact  the  resulting  increase  in  expectation 
of  life  falls  seven  years  short  of  ichat  might  reasonably 
he  expected  to  folloiv  the  selection  of  only  one  generation 
of  ancestry  {the  parental)  for  longevity. 

So  much  for  BelFs  analysis  of  longevity  in  the  Hyde 


166  BIOLOGY  OF  DEATH 

family.  "We  have  seen  that  it  demonstrates  with  the  ut- 
most clearness  and  certainty  that  there  is  an  hereditary 
influence  between  parent  and  offspring  affecting  the  ex- 
pectation of  longevity  of  the  latter.  Bell's  method  of 
handling  the  material  does  not  proyide  any  precise  meas- 
ure of  the  intensity  of  this  hereditary  influence,  nor  does 
it  furnish  any  indication  of  its  strength  in  any  but  the 
direct  line  of  descent.  Of  course,  if  heredity  is  a  factor 
in  the  determination  of  longevity  we  should  expect  its 
effects  to  be  manifested  as  between  brothers  and  sisters, 
or  in  the  avuncular  relationships,  and  in  greater  or  less 
degree  in  all  the  other  collateral  and  more  remote  direct 
degrees  of  kinsliip.  Happily,  we  have  a  painstaking 
analysis,  with  a  quantitative  measure  of  the  relative  in- 
fluence of  heredity  in  the  determination  of  longevity, 
which  was  carried  out  many  years  before  Bell's  work  on 
the  Hyde  family,  by  the  pioneer  in  this  field.  Prof.  Karl 
Pearson.  His  demonstration  of  the  inheritance  of  longev- 
ity appeared  more  than  twenty  years  before  that  of 
Bell.  I  have  called  attention  to  the  latter 's  work  first 
merely  because  of  the  greater  simplicity  and  directness  of 
his  demonstration.  We  may  now  turn  to  a  consideration 
of  Pearson's  more  detailed  results. 

Pearson's  work 

The  material  used  by  Pearson  and  his  student,  Miss 
Beeton,  who  worked  with  him  on  the  problem,  came  from 
a  number  of  different  sources.  Their  first  study  dealt 
with  three  series  from  which  all  deaths  recorded  as  due 
to  accident  were  excluded.  The  first  series  included  one 
thousand  cases  of  the  ages  of  fathers  and  sons  at 
death,  the  latter  being  over  22.5  years   of  age,  taken 


THE  INHERITANCE  OF  DURATION         1G7 

from  Foster's  '^Peerage."  The  second  series  consisted 
of  a  thousand  pairs  of  fathers  and  sons,  the  hitter 
dying  beyond  the  age  of  20,  taken  from  Rurke's 
'^Landed  Gentry."  The  third  series  consisted  of  ages 
at  death  of  one  thousand  pairs  of  Ijrotlicrs  dying 
beyond  the  age  of  20  taken  from  the  ^'Peerage."  It 
will  be  noted  that  all  these  series  considered  in  this  first 
studv  dealt  only  with  inheritance  in  the  male  line.  Tlio 
reason  for  this  was  simply  that  in  such  books  of  record 
as  the  ^* Peerage"  and  ^^ Landed  Gentry"  sufficiently  ex- 
act account  is  not  given  of  the  deaths  of  female  relatives. 
In  a  second  study  the  material  was  taken  from  the  pedi- 
gree records  of  members  of  the  English  Society  of  Friends 
and  from  the  Friends'  Provident  Association.  This  ma- 
terial included  data  on  inheritance  of  longevity  in  the 
female  line  and  also  provided  data  for  deaths  of  infants, 
which  were  lacking  in  the  earlier  used  material.  The 
investigation  was  grounded  upon  that  important  branch 
of  modern  statistical  calculus  kno\\Ti  as  the  method  of 
correlation.  For  each  pair  of  relatives  between  whom  it 
was  desired  to  study  the  intensity  of  inheritance  of  longe- 
vity a  table  of  double  entry  was  formed,  like  the  one  shown 
here  as  Table  17. 

The  figures  in  each  cell  or  compartment  of  this  table 
denote  the  frequency  of  occurrence  of  pairs  of  fathers 
and  adult  sons  having  respectively  the  durations  of  life 
indicated  by  the  figures  in  the  margins.  Thus  we  see, 
examining  the  first  line  of  the  table,  that  there  were  1 1 
cases  in  which  the  average  duration  of  life  of  the  father 
was  48  years  and  that  of  the  adult  son  23  years.  Farther 
down  and  to  the  right  in  the  table  there  were  13  cases  in 
which  the  average  duration  of  life  of  the  father  and  the 
son  was  in  each  case  83  years.     These  cases  are  men- 


168 


BIOLOGY  OF  DEATH 


tioned  merely  as  illustrations.     The  whole  table  is  to  be 
read  in  the  same  manner. 

From  such  a  table  as  this  it  is  possible  to  calculate, 
by  well-known  mathematical  methods,  a  single  numerical 
constant  of  somewhat  unique  properties  known  as  the 

TABLE  17 

Correlation  table  showing  the  correlation  between  father  and  son  in  respect 

of  duration  of  life 

DURATION  OP  LIFE  OF  FATHER 


23 

28 

33 

38 

43 

48 

53 

58 

63 
11 

68 

73 

78 

83 

88 

93 

98 

103 

Totals 

23 

1 

1 

2 

5 

3 

11 

6 

7 

9 

6 

12 

8 

2 

2 

86 

28 

1 

6 

4 

5 

12 

15 

10 

13 

10 

7 

1 

1 

85 

§    33 

1 

2 

2 

5 

7 

8 

7 

10 

7 

8 

8 

4 

1 

70 

«^    38 

1 

1 

2 

2 

8 

5 

3 

9 

11 

11 

9 

5 

2 

1 

70 

^    43 

1 

1 

5 

1 

5 

6 

11 

10 

10 

17 

5 

72 

H    48 

1 

1 

2 

5 

5 

4 

6 

9 

12 

15 

5 

3 

68 

S    53 

1 

3 

5 

7 

3 

2 

11 

11 

14 

10 

1 

1 

1 

70 

^    58 

1 

3 

4 

5 

10 

8 

10 

5 

8 

9 

3 

2 

68 

§    63 
Z        68 

2 

1 

3 

5 

1 

4 

8 

13 

9 

11 

11 

11 

5 

84 

1 

6 

3 

6 

7 

5 

5 

6 

14 

16 

12 

7 

2 

90 

1    73 

1 

2 

1 

6 

5 

4 

7 

9 

10 

14 

13 

8 

8 

1 

1 

90 

H    78 

1 

1 

2 

2 

4 

4 

4 

10 

5 

8 

9 

4 

3 

57 

«    83 

1 

1 

5 

3 

1 

2 

3 

7 

10 

13 

3 

2 

2 

53 

§    88 

1 

2 

3 

1 

4 

7 

5 

1 

2 

2 

28 

""        93 

1 

2 

2 

5 

98 

1 

1 

1 

1 

4 

Totals 

1 

8 

9 

30 

26 

65 

70 

76 

90 

122 

131 

153 

132 

53 

18 

15 

1 

1000 

coefficient  of  correlation,  which  measures  the  degree  of 
association  or  mutual  dependence  of  the  two  variables 
included  in  such  double  entry  tables.  This  coefficient 
measures  the  amount  of  resemblance  or  association  be- 
tween characteristics  of  individuals  or  things.  It  is 
stated  in  the  form  of  a  decimal  which  may  take  any  value 
between  0  and  1.  As  the  correlation  coefficient  rises  to 
1  we  approach  a  condition  of  absolute  dependence  of  the 
variables  one  upon  the  other.  As  it  falls  to  zero 
we  approach  a  condition  of  absolute  independence,  where 
the  one  variable  has  no  relation  to  the  other  in  the  amount 


THE  INHERITANCE  OF  DURATION 


169 


or  direction  of  its  variation.  The  significance  of  a  cor- 
relation coefficient  is  always  to  be  judged,  in  any  partic- 
ular case,  by  the  magnitude  of  a  constant  associated 
with  it  called  the  probable  error.  A  correlation  coeffi- 
cient may  be  regarded  as  certainly  significant  when  it  has 
a  value  of  4  or  more  times  that  of  its  prol)al)le  error, 
which  is  always  stated  after  the  coefficient  with  a  com- 
bined plus  and  minus  sign  between  the  two.  The  coeffi- 
cient is  probably  significant  when  it  has  a  value  of  not 
less  than  3  times  its  probable  error.  By  ''significant'' 
in  this  connection  is  meant  that  the  coefficient  probably 
is  not  merely  a  random  chance  result. 

In  Table  18  are  the  numerical  results  from  the  first 
study  based  upon  the  ''Peerage"  and  "Landed  Gentry." 

TABLE  18 

Inheritance  of  duration  of  life  in  male  line.     Data  from  "Peerage"  and 
*' Landed  Gentry."     (Beef on  and  Pearson). 


natio  of 

Relatives 

Correlation 

coefficient  to 

coeflBcient 

its  probable 

'•xy 

error 

X 

y 

'ry    -^  ^r 

Father  ("Peerage") 

Son,  25  years  and  over 

.115  ±.021 

5.5 

Father  ("Landed  Gentry") 

Son,  20  years  and  over 

.142  ±.021 

6.8 

Father  ("Peerage") 

Son,  52.5  years  and  over 

.116  ±.023 

5.0 

Father  ("Landed  Gentry") 

Son,  50  years  and  over 

.113  ±.024 

4.7 

Brother  ("Peerage") 

Brother 

.260  ±  .020 

13.0 

It  is  seen  at  once  that  all  of  the  coefficients  are  signifi- 
cant in  comparison  with  their  probable  errors.  The 
last  column  of  the  table  gives  the  ratio  of  the  coefficient 
to  its  probable  error,  and  in  the  worst  case  the 
coefficient  is  4.7  times  its  probable  error.  The  odds 
against  such  a  correlation  having  arisen  from  chance 
alone  are  about  655  to  1.  Odds  such  as  these  may 
be  certainly  taken  as  demonstrating  that  the  results  rep- 


170  BIOLOGY  OF  DEATH 

resent  true  organic  relationship  and  not  mere  chance. 
All  of  the  other  coefficients  are  certainly  significant,  hav- 
ing regard  to  their  probable  errors.  Furthermore,  they 
are  all  positive  in  sign,  which  implies  that  a  variation  in 
the  direction  of  increased  duration  of  life  in  one  relative 
of  the  pair  is  associated  with  an  increase  in  expectation 
of  life  in  the  other.  It  will  be  noted  that  the  magnitude 
of  the  correlation  between  brother  and  brother  is  about 
twice  as  great  as  in  the  case  of  correlation  of  father  with 
son.  From  this  it  is  provisionally  concluded  that  the 
intensity  of  the  hereditary  influence  in  respect  of  duration 
of  life  is  greater  in  the  fraternal  relationship  than  in  the 
parental.  It  evidently  makes  no  difference,  broadly 
speaking,  so  far  as  these  two  sets  of  material  are  con- 
cerned, whether  there  are  included  in  the  correlation  table 
all  adult  sons,  whatever  their  age,  or  only  adult  sons  over 
50  years  of  age.  The  coefficients  in  both  cases  are  es- 
sentially of  the  same  order  of  magnitude. 

Perhaps  someone  will  be  inclined  to  believe  that  the 
correlation  between  father  and  son,  and  brother:  and 
brother,  in  respect  of  the  duration  of  life  arises  as  a 
result  of  similarity  of  the  environments  to  which  they 
are  exposed.  Pearson's  comments  on  this  point  are 
penetrating,  and  I  believe  absolutely  sound.     He  says : 

There  may  be  some  readers  who  will  be  inclined  to  consider  that  much 
of  the  correlation  of  duration  of  life  between  brothers  is  due  to  there  being 
a  likeness  of  their  environment,  and  that  thus  each  pair  of  brethren  is 
linked  together  and  differentiated  from  the  general  population.  But  it  is 
difficult  to  believe  that  this  really  affects  adult  brothers  or  a  father  and  his 
adult  offspring  A  man  who  dies  between  40  and  80  can  hardly  be  said 
to  have  an  environment  more  like  that  of  his  brother  or  father,  who  died 
also  at  some  such  age.  than  like  any  other  member  of  the  general  popula- 
tion. Of  course,  two  brothers  have  usually  a  like  environment  in  infancy, 
and  their  ages  at  death,  even  if  they  die  adults,  may  be  influenced  by  their 
rearing.     But  if  this  be  true,  we  ought  to  find  a  high  correlation  in  ages 


THE  INHERITANCE  OF  DURATION 


171 


at  death  of  brethren  who  die  as  minors.  As  a  matter  of  fact  this  correhi- 
tion  for  minor  and  minor  is  40  to  50  per  cent,  less  tlum  in  the  case 
of  adult  and  adult.  It  would  thus  seem  that  identity  of  environment  iH 
not  the  principal  factor  in  the  correlation  Ijetween  ages  of  death,  for  thia 
correlation  is  far  less  in  youth  tlian  in  old  age. 

TABLE  19 

Inheritance  of  duration  of  life.     Data  from  Quaker  records. 

{Beeton  and  Pearson) 


Relatives 

Correlation 
coefficient 

Ratio  of 

coefficient  to  it« 

probable  error 

X 

y 

'ry 

Father 

Adult  son 

0.135  ±  .021 

6.4 

Father 

Minor  son 

.087  ±  .022 

4.0 

Father 

Adult  daughter 

.130±  .020 

6.5 

Father 

Minor  daughter 

.052  ±  .023 

2.3 

Mother 

Adult  son 

.131  ±  .019 

6.9 

Mother 

Minor  son 

.076  ±  .024 

3.2 

Mother 

Adult  daughter 

.149±  .020 

7.5 

Mother 

Minor  daughter 

.13S=b  .024 

5  7 

Elder  adult  brother 

Younger  adult  brother 

.229  db  .019 

12.1 

Adult  brother 

Adult  brother 

.285  ±  .020 

14.3 

Minor  brother 

Minor  brother 

.103  db  .029 

3  6 

Adult  brother 

Minor  brother 

-.026  it  .025 

1.0 

Elder  adult  sister 

Younger  adult  sister 

.346  ±  .018 

19.2 

Adult  sister 

Adult  sister 

.332  ±  .019 

17.5 

Minor  sister 

Minor  sister 

.175  ±  .031 

5.6 

Adult  sister 

Minor  sister 

-.026  ±  .029 

.9 

Adult  brother 

Adult  sister 

.232  ±  .015 

15.5 

Minor  brother 

Minor  sister 

.144=t  .025 

5.8 

Adult  brother 

Minor  sister 

-.006  ±  .035 

.2 

Adult  sister 

Minor  brother 

-.027  ±  .024 

1.1 

The  cases  above  the  horizontal  line  are  all  direct  lineal   inheritance; 
those  below  the  line  collateral  inheritance. 


The  results  regarding  minors  to  which  Pearson  refers 
are  showTi  in  Table  19.  This  table  gives  the  re.sults  of 
the  second  study  made  by  Beeton  and  Pearson  on  inher- 
itance of  duration  of  life,  based  upon  the  records  of  the 


172  BIOLOGY  OF  DEATH 

Friends'  Societies.  It  appears  in  the  upper  half  of  the 
table  that  wherever  a  parent,  father  or  mother,  appears 
with  a  minor  son  or  daughter  the  correlation  coefficients 
are  small  in  magnitude.  In  some  cases  they  are  just 
barely  significant  in  comparison  with  their  probable  errors 
as  for  example,  the  correlation  of  father  and  minor 
son,  and  that  of  mother  and  minor  daughter.  In  the 
other  cases  involving  minors  the  coefficients  are  so  small 
as  to  be  insigTiificant.  On  the  other  hand,  in  every  case 
of  correlation  between  parent  and  adult  offspring  of 
either  sex,  the  coefficient  is  6  or  more  times  its  probable 
error,  and  must  certainly  be  regarded  as  significant.  It 
will  further  be  noted  that  the  magnitude  of  the  coefficients 
obtained  from  these  Quaker  records,  is  of  the  same  general 
order  as  was  seen  in  the  previous  table  based  on  the 
^^ Peerage''  and  *' Landed  Gentry"  material. 

The  lower  part  of  the  table  gives  the  results  for 
various  fraternal  relationships.  In  general  the  frater- 
nal correlations  are  higher  that  the  parental.  The  coeffi- 
cients for  minors  or  for  minors  with  adults  are  very  low 
and  in  most  cases  not  significantly  different  from  zero. 
In  four  cases — namely,  adult  brother  w^th  minor  brother ; 
adult  sister  with  minor  sister ;  adult  brother  with  minor 
sister;  and  adult  sister  with  minor  brother — the  coeffi- 
cients are  all  negative  in  sign,  although  in  no  one  of  the 
cases  is  the  coefficient  significant  in  comparison  with 
its  probable  error.  A  minus  sign  before  a  correlation 
coefficient  means  that  an  increase  in  the  value  of 
one  of  the  variables  is  associated  with  a  decrease 
in  the  value  of  the  other.  So  that  these  negative 
coefficients  would  mean,  if  they  were  significant,  that 
the  greater  the  age  at  death  of  an  adult  brother,  the  lower 
the  age  at  death  of  his  minor  brother  or  sister.  But  the 
coefficients  are  actually  sensibly  equal  to  zero.     Pearson 


THE  INHERITANCE  OF  DURATION         173 

points  out  that  the  minus  sigii  in  the  case  of  these  correla- 
tions of  adult  with  minor  exhibits  the  effect  of  the  inheri- 
tance of  the  mortality  of  youth.  Minors  dyin^^  from  IG 
to  20  are  associated  with  adults  dying  from  21  to  25. 
That  is,  minors  dying  late  correspond  to  adults  dying 
early.  This  situation  may  be  a  peculiarity  of  the  Quaker 
material  with  which  tliis  work  deals.  There  is  urgent 
need  for  further  study  of  the  inheritance  of  the  duration 
of  life  on  more  and  better  material  than  any  which  has 
hitherto  been  used  for  the  purpose.  I  have  under  way 
in  my  own  laboratory  at  the  present  time  an  extensive 
investigation  of  this  kind,  in  which  there  will  be  hundreds 
of  thousands  of  pairs  of  relatives  in  the  individual 
correlation  tables  instead  of  thousands,  and  all  types  of 
collateral  kinsliip  will  be  represented.  Because  of  the 
magnitude  of  the  investigation,  however,  it  will  be  still 
a  number  of  years  before  the  results  will  be  in  hand 
for  discussion. 

The  facts  which  have  been  presented  leave  no  doubt 
as  to  the  reality  of  the  inheritance  factor  as  a  prime 
determinant  of  the  length  of  the  life  span. 

At  the  beginning  it  was  pointed  out  that  it  was  on 
a  priori  grounds  highly  probable  that  duration  of  life 
is  influenced  by  both  heredity  and  environment,  and  that 
the  real  problem  is  to  measure  the  comparative  effect  of 
these  two  general  sets  of  factors.  'We  have  seen  that  the 
intensity  of  inheritance  of  duration  of  life,  taking  aver- 
ages, is  of  the  order  indicated  by  the  following  coefficients. 

Parental  correlation  (adult  children)  r  =  .  1365 
Fraternal  correlation  (adults)  r=.2831 

Now  we  have  to  ask  this  question :  What  are  the  values 
of  parental  and  fraternal  correlation  for  characters  but 
slightly  if  at  all  affected  in  their  values  by  the  environ- 
ment? Happily,  Pearson  has  provided  such  values  in  liis 


174  BIOLOGY  OF  DEATH 

extensive  investigations  on  the  inheritance  of  physical 
characters  in  man. 

In  Table  20  are  given  the  values  of  the  parental 
correlations  for  the  four  physical  characters — stature, 
span,  forearm  length,  and  eye  color.     Now  it  is  ob\dous 

TABLE  20 

Parental  inheritance  of  physical  characters  in  man.     (Pearson) 

Pair  Organ  Correlation 

Father  and  Son Stature .51 

Father  and  Son Span 45 

Father  and  Son Forearm .42 

Father  and  Son Eye  color .55 

Father  and  Daughter Stature 51 

Father  and  Daughter Span .45 

Father  and  Daughter Forearm 42 

Father  and  Daughter Eye  color 44 

Mother  and  Son Stature .49 

Mother  and  Son Span .46 

Mother  and  Son Forearm .41 

Mother  and  Son Eye  color .48 

Mother  and  Daughter Stature .51 

Mother  and  Daughter Span .45 

Mother  and  Daughter Forearm .42 

Mother  and  Daughter Eye  color .51 

that  the  differences  of  environmental  forces  impinging 
upon  the  various  members  of  a  homogeneous  group  of 
middle  class  English  families  (from  which  source  the 
data  for  these  correlations  were  drawn)  can  by  no  pos- 
sibility be  great  enough  to  affect  sensibly  the  stature,  the 
arm-length,  or  the  eye  color  of  the  adults  of  such  families. 
It  would  be  preposterous  to  assert  that  the  resemblance 
between  parents  and  offspring  in  respect  of  eye  color  is 
due  solely,  or  even  sensibly,  to  similarity  of  environment. 
It  is  due  to  heredity  and  substantially  nothing  else. 
Now  the  average  value  of  the  16  parental  coefficients  for 
the  inheritance  of  physical  characters  sho^vn  in  the  table  is 

r=  .4675 


THE  INHERITANCE  OF  DURATION         175 

Table  21  shows  the  coefTicients  for  the  fraternal  in- 
heritance of  six  physical  characters,  cephalic  index  (the 
ratio  of  head  length  and  head  breadtli)  and  hair  color 
having  been  added  to  those  given  in  the  parental  table. 
Again  it  is  seen  that  the  coefficients  have  all  about  the 

TABLE  21 

Fraternal  inheritance  of  physical  characters  in  man.     (Pearson) 

Pair  Organ  CorrelatioD 

Brother  and  Brother Stature .51 

Brother  and  Brother Span .55 

Brother  and  Brother Forearm .49 

Brother  and  Brother Eye  color 52 

Brother  and  Brother CephaHc  index 49 

Brother  and  Brother Hair  color .59 

Sister  and  Sister Stature 54 

Sister  and  Sister Span .56 

Sister  and  Sister Forearm .51 

Sister  and  Sister Eye  color .45 

Sister  and  Sister Cephalic  index .54 

Sister  and  Sister Hair  color .56 

Brother  and  Sister Stature .55 

Brother  and  Sister Span .53 

Brother  and  Sister Forearm .44 

Brother  and  Sister Eye  color .46 

Brother  and  Sister Cephahc  index .43 

Brother  and  Sister Hair  color .56 

same  values,  and  it  is  as  apparent  as  before  that  the 
resemblance  between  brother  and  sister,  for  example,  in 
eye-color,  or  arm  length,  or  shape  of  head  cannot  for 
a  moment,  because  of  the  nature  of  the  characters  them- 
selves, be  supposed  to  have  arisen  because  of  the  simi- 
larity of  environment.  The  average  value  of  all  these 
fraternal  coefficients  is 

r=.5156 

From  these  data,  with  the  help  of  a  method  due  to 
Pearson,  it  is  possible  to  determine  the  percentage  of  the 


176  BIOLOGY  OF  DEATH 

death  rate  dependent  upon  the  inherited  constitution,  and 
the  percentage  not  so  dependent.  If  pN  be  the  number 
of  deaths  in  N  cases  which  depend  in  no  way  upon  the 
inherited  constitution  of  the  individual,  then  (l-p)  will 
represent  the  chance  of  an  individual  dying  because  of 
his  inherited  constitutional  makeup,  and  (1-p)^  will  be 
the  chance  of  a  pair  of  individuals,  say  two  brothers,  both 
dying  from  causes  determined  by  inheritance.  If  further 
r  denotes  the  observed  correlation  between  individuals  in 
respect  of  duration  of  life,  and  Tq  the  correlation  between 
the  same  kin  in  respect  of  such  measured  physical  charac- 
ters as  those  just  discussed,  in  the  determination  of  which 
it  is  agreed  that  environment  can  play  only  a  small  part, 
we  have  the  following  relation: 

To 

Substituting  the  ascertained  values  we  have 

1.  From  parental  correlations. 

0.1365  =  .4675  (l-p)  ^ 

(l-p)  2  =  .292 

(l-p)  =  .54 

2.  From  fraternal  correlations 

0.2831  =  .5156  (l-p)  2 
(l-p)  =  .74 

From  these  figures  it  may  be  concluded,  and  Pearson 
does  so  conclude,  that  from  50  to  75  per  cent,  of  the 
general  death  rate  within  the  group  of  the  population  on 
which  the  calculations  are  based,  is  determined  funda- 
mentally by  factors  of  heredity  and  is  not  capable  of 
essential  modification  or  amelioration  by  any  sort  of 
environmental  action,  however  well  intentioned,  however 
costly,  or  however  well  advertised.  Mutatis  mutandis 
the  same  conclusion  applies  to  the  duration  of  Life.    I  have 


THE  INHERITANCE  OF  DURATION  177 

preferred  to  state  the  conclusion  in  terms  of  death  rates, 
as  it  was  originally  stated  by  Pearson,  because  of  tlie 
bearing  it  has  upon  a  great  deal  of  the  public  health 
propaganda  so  loosely  flung  about.  It  need  only  be  re- 
membered that  there  is  a  perfectly  definite  functional 
relation  between  death  rate  and  average  duration  of  life 
in  an  approximately  stable  population  group,  expres- 
sible by  an  equation,  in  order  to  see  that  any  conclusion 
as  to  the  relative  influence  of  heredity  and  environment 
upon  the  general  death  rate  must  apply  with  equal  force 
to  the  duration  of  life. 

THE  SELECTIVE  DEATH  RATE  IN  MAN 

If  the  duration  of  life  were  inherited  it  would  logical- 
ly be  expected  that  some  portion  of  the  death  rate  must 
be  selective  in  character.  For  inheritance  of  duration 
of  life  can  only  mean  that  when  a  person  dies  is  in  part 
determined  by  that  individual's  biological  constitution  or 
makeup.  And  equally  it  is  obvious  that  individuals  of 
weak  and  unsound  constitution  must,  on  the  average, 
die  earlier  than  those  of  strong,  sound,  and  vigorous  con- 
stitution. Whence  it  follows  that  the  chances  of  leaving 
offspring  will  be  greater  for  those  of  sound  constitution 
than  for  the  weaklings.  The  mathematical  discussion 
which  has  just  been  given  indicates  that  from  one-half 
to  three-fourths  of  the  death  rate  is  selective  in  char- 
acter, because  that  proportion  is  determined  by  hereditary 
factors.  Just  in  proportion  as  heredity  determines 
the  death  rate,  so  is  the  mortality  selective.  The  reality  of 
the  fact  of  a  selective  death  rate  in  man  can  be  easily 
shown  graphically. 

In  Figure  44  are  seen  the  graphs  of  some  data  from 
European  royal  families,  where  no  neglect  of  children, 

12 


178 


BIOLOGY  OF  DEATH 


degrading  environmental  conditions,  or  economic  want 
can  have  influenced  the  results.     These  data  were  com- 


:E 


6 


SO 


45 


40 


35 


15 


10 


MOTHER   AND    CHILDREN 
FAIHLR  AND    CHILDRLN 


16 


16 


36 


45 


56 


66 


76 


&6  and  o\/er 


AGL    AT     DEATH     OF    PARENTS 


Fia.  44. — Diagram  showing  the  influence  of  age  at  death  of  parents  upon  the  percentage  of 

offspring  dying  under  5  years.     (After  Ploetz). 

piled   by   the  well-known   German   eugenist,   Professor 
Ploetz    of   Munich.     The    lines    show   the    falling   per- 


THE  INHERITANCE  OF  DURATION         179 

centage  of  the  infantile  death  rate  as  the  duration  of 
life  of  the  father  and  mother  increases.  Amon^  tho  chil- 
dren of  short-lived  fathers  and  mothers,  at  the  left  end 
of  each  line,  is  found  the  highest  infant  mortality,  while 
among  the  offspring  of  long-lived  parents  tho  lowest 
infant  mortality  occurs,  as  shown  at  the  right-hand  end  of 
the  diagram. 

The  results  so  far  presented  regarding  a  selective 
death  rate  and  inheritance  of  duration  of  life,  have  come 
from  selected  classes :  the  aristocracy,  royalty  or  Quakers. 
None  of  these  classes  can  be  fairly  said  to  represent  the 
general  population.  Can  the  conclusion  be  transferred 
safely  from  the  classes  to  the  masses?  To  the  determina- 
tion of  this  point  one  of  Pearson's  students,  Dr.  E.  C.  Snow, 
addressed  himself.  The  method  which  he  used  w^as,  from 
the  necessities  of  the  case,  a  much  more  complicated  and 
indirect  one  than  that  of  Pearson  and  Ploetz.  Its  essen- 
tial idea  was  to  see  whether  infant  deaths  w^eeded  out  the 
unfit  and  left  as  survivors  the  stronger  and  more  resis- 
tant. All  the  infants  born  in  a  single  year  were  taken 
as  a  cohort  and  the  deaths  occurring  in  this  cohort  in  suc- 
cessive years  were  followed  through.  Resort  was  had 
to  the  method  of  partial  or  net  correlation.  The  variables 
correlated  in  the  case  of  the  Prussian  data  were  these : 

1.  a?„  =  Births  in  year     a  given  cohort  started. 

2.  a?i  =  Deaths  in  the  first  two  years  of  life. 

3.  X2  =  Deaths  in  the  next  eight  years  of  life. 

4.  fPj  =  Deaths  in  the  ten  years  of  all   individuals  not   included   in 

the  particular  cohort  whose  deaths  are  being  followed. 

In  the  case  of  the  English  data  the  varialilos  were: 

a?o  =  Births  in  specified  year. 

Xi  =  Deaths  in  the    first    three    years    of    life    of    those    l)orn    in 

specified  year. 
X2  =■  Deaths  in  fourth   and    fifth    years   of   life  of   those   born    in 

specified  year. 
Xi  =:  The  "remaining"  deaths  under  5. 


180 


BIOLOGY  OF  DEATH 


The  underlying  idea  was  to  get  the  partial  or  net 
correlation  between  x^  and  X2,  while  Xq  and  x^  are  held 
constant.  If  the  mortality  of  infancy  is  selective,  its 
amount  should  be  negatively  correlated  to  a  significant 
degree  with  the  mortality  of  the  next  eight  years  when 
the  births  in  each  district  considered  are  made  con- 
stant and  when  the  general  health  environment  is  made 
constant.  Under  the  constant  conditions  specified  a 
negative  correlation  denotes  that  the  heavier  the  infan- 


TABLE  22 

Snow^s  results  on  selective  death  rate  in  man. 

rural  districts 


English  and  Prussian 


Data 

Actual  correlation 
^12.03 

Expected  correlation 
if  no  selection 

Males: 

English  Rural 
Districts 

(1870) 
(1871) 
(1872) 

-0.4483 

-  .3574 

-  .2271 

-0.0828 

-  .1014 

-  .0807 

Prussian  Rural 
Districts 

(1881) 
(1882) 

-  .9278 

-  .6050 

-  .0958 

-  .0765 

Females : 

English  Rural 

Districts 

(1870) 
(1871) 
(1872) 

-  .4666 

-  .2857 

-  .5089 

-  .0708 

-  .0505 

-  .0496 

Prussian  Rural 
Districts 

(1881) 

(1882) 

-  .8483 

-  .6078 

-  .0933 

-  .0705 

tile  death  rate  in  a  cohort  of  births  the  lighter  will  be 
the  death  rate  of  later  years,  and  vice  versa.  The  last 
variable,  x^,  is  the  one  chosen,  after  careful  consideration 
and  many  trials,  to  measure  variation  in  the  health  envi- 
ronment. If  any  year  is  a  particularly  unhealthy  one — an 
epidemic  year  for  example — then  this  unhealthiness 
should  be  accurately  reflected  in  the  deaths  of  those  mem- 
bers of  the  population  not  included  in  the  cohort 
under  review. 


THE  INHERITANCE  OF  DURATION         181 

Snow's  results  for  English  and  Prussian  rural  dis- 
tricts are  set  forth  in  Table  22.  From  this  table  it  is 
seen  that  in  every  case  the  correlations  are  negative,  and 
therefore  indicate  that  the  mortality  of  early  life  is  selec- 
tive. Furthermore,  the  demonstration  of  this  fact  is 
completed  by  showing  that  the  observed  coefficients  are 
from  3  to  10  times  as  great  as  they  would  be  if  there  were 
no  selective  character  to  the  death  rate.  Tlie  coefficients 
for  the  Prussian  population,  it  will  be  noted,  are  of  a 
distinctly  higher  order  of  magnitude  than  those  for  the 
English  population.  Tliis  divergence  is  probably  due 
chiefly  to  differences  in  the  quality  of  the  fundamental 
statistical  material  in  the  two  cases.  The  Prussian  ma- 
terial is  free  from  certain  defects  inherent  in  the  English 
data,  which  camiot  be  entirely  got  rid  of.  The  difference 
in  the  coefficients  for  the  two  successive  Prussian  cohorts 
represents,  in  Snow's  opinion,  probably  a  real  fluctua- 
tion in  the  intensity  of  natural  selection  in  the  one  group 
as  compared  with  the  other.  How  significant  Snow's 
results  are  is  sho^vai  gTapliically  in  Figure  45. 

Snow's  own  comments  on  liis  results  are  significant. 
He  says: 

The  investigations  of  this  memoir  have  been  long  and  laborious,  and 
the  difficulties  presented  by  the  data  have  been  great.  Still,  the  general 
result  cannot  be  questioned.  Natural  selection,  in  the  form  of  a  selective 
death-rate,  is  strongly  operative  in  man  in  the  early  years  of  life.  Those 
data  which  we  believe  to  be  the  best  among  those  we  have  used — the  Prus- 
sian figures — show  very  high  negative  correlation  between  the  deaths  in 
the  first  two  years  of  life  and  those  in  the  next  eiglit,  when  allowiincf  is 
made  for  difference  in  environment.  We  assert  with  great  contideuce  that 
a  high  mortality  in  infancy  (the  first  two  years  of  life)  is  followed  by  a 
corresponding  low  mortality  in  childhood,  and  conversely.  The  English 
figures  do  not  allow  such  a  comprehensive  survey  to  be  undertaken,  but, 
so  far  as  they  go,  they  point  in  the  same  direction  as  the  Prussian  ones. 
The  migratory  tendencies  in  urban  districts  militate  again.st  the  detection 
of  selective  influences  there,  but  we  express  the  belief  that  those  influences 


182 


BIOLOGY  OF  DEATH 


are  just  as  prevalent  in  industrial  as  in  rural  communities,  and  could  be 
measured  by  other  means  if  the  data  were  forthcoming. 


LO  r- 


^ 


s 


o 


^ 


fc 


b 


I 


§5 


.J- 


.4- 


.3 


.£ 


./ 


.0 


MALES 


EXPECTED    COR  RELATION  ■  NO  SELECTION 


1670 


1671 


1672 


/SSI 


1632 


ENGLISH 


PRUSSIAN 


Fio.  45. — Snow's  results  on  selective  death  rate  in  man.  The  cross-hatched  area  may 
be  taken,  in  comparison  with  the  small  clear  area  at  the  bottom,  as  indicating  the  influence 
of  the  selective  death  rate  in  increasing  the  correlations. 

Our  investigation  substantiates  for  a  general   population  the  results 
found  by  Pearson  and  Ploetz  for  more  restricted  populations,  and  disagrees 

It  is  with  great  reluctance  that 


with  many  statements  of  health  officers. 


THE  INHERITANCE  OF  DURATION         183 

we  point  out  this  disagreement,  and  aspert  a  doctrine  which,  in  the  present 
sentiment  of  society,  is  bound  to  be  unpopular.     We  have  no   foclinKR  of 
antagonism  towards  the  efforts  which  have  been  made  in  recent  years  to 
save  infant  life,  but  we  think  that  the  probable  consequences  of  such  actions, 
BO  far  as  past  experience  can  indicate  them,  should  be  completely  under- 
stood.    All  attempts  at  the  reduction  of  mortality  of  infancy  and  childhood 
should  be  made  in  the  full  knowledge  of  the  facts  of  heredity.     EverylKxiy 
knows  the  extreme  differences  in  constitutional  fitness  which  exist  in  men 
and  women.     Few  intelligent  people  can  be  ignorant  of  the  fact  that  thi.^ 
constitutional    fitness    is    inherited    according    to    laws    which    are    fairly 
definitely  known.     At  the  same  time  marriage  is  just  as  prevalent  among 
those  of  weak  stocks  as  among  those  of  the  vigorous,  while  the  fertility 
of  the  former  is  certainly  not  less  than  that  of  the  latter.     Thus  a  propor- 
tion of  the  infants  born  every  year  must  inevitably  belong  to  the  class 
referred  to  in  the  report  as  "weaklings,"  and,  with  Pearson's  results  before 
us,  we  are  quite  convinced  that  true  infantile  mortality   (as  distinct  from 
the  mortality  due  to  accident,   neglect,   etc.— no   small   proportion   of   the 
whole)    finds  most  victims  from  among  this  class.     Incidentally  we  would 
here   suggest  that  no  investigation   into  the   causes   of    infant   and   child 
mortality  is  complete  until  particulars  are  gathered  by  the  medical  officers 
of  the  constitutional  tendencies  and  physical  characters  of  the  parents. 

Our  work  has  led  us  to  the  conclusion  that  infant  mortality  docs  effect 
a  "weeding  out"  of  the  unfit;  but,  though  we  would  give  this  conclusion 
all  due  emphasis,  we  do  not  wish  to  assert  that  any  effort,  however  small, 
to  the  end  of  reducing  this  mortality  is  undesirable.  Nobody  would  suggest 
that  the  difference  between  the  infant  rates  in  Oxfordshire  and  Glamorgan- 
shire (73  and  154  per  1,000  births  respectively,  in  1908)  was  wholly  due 
to  the  constitutional  superiority  of  the  inhabitants  of  the  former  county. 
The  "w3eding-out"  process  is  not  uniform.  In  the  mining  districts  of 
South  Wales,  accident,  negligence,  ignorance  and  insanitary  surroundings 
account  for  much.  By  causing  improvements  under  these  heads  it  may 
bo  possible  to  reduce  the  infant  mortality  of  Glamorganshire  b^  the  sur- 
vival of  many  who  are  not  more  unfit  than  are  those  who  survive  in 
Oxfordshire,  and  the  social  instincts  of  the  community  insist  that  this 
should  be  done. 

This  work  of  Snow's  aroused  great  interest,  and  soon 
after  it  appearance  was  controverted,  as  it  seems  to  me 
quite  unsuccessfully,  by  Brownlee,  Salee])y  and  others. 

Happily  the  results  of  Pearson,  Ploetz  and  Snow  on 
the  selective  death  rate  have  recently  been  accorded  a 
confirmation  and   extension   to  still   another   group   of 


184  BIOLOGY  OF  DEATH 

people — the  Dutch — in  some  investigations  carried  out 
by  Dr.  F.  S.  Crum  of  the  Prudential  Life  Insurance  Com- 
pany, with  the  assistance  of  the  distinguished  mathe- 
matical statistician,  Mr.  Arne  Fisher. 

The  Dutch  Government  publishes  annually  data  which 
undoubtedly  furnish  the  best  available  material  now  exist- 
ing in  the  world  for  the  purpose  of  determining  whether 
or  not  there  is  a  positive  or  negative  correlation  between 
infant  mortality  and  the  mortality  in  the  immediately 
subsequent  years  of  life.  Fisher's  mathematical  analy- 
sis embraces  a  very  large  body  of  material,  including 
nearly  a  million  and  a  half  births,  and  nearly  a  quarter 
of  a  million  deaths  of  males  occurring  in  the  first  five 
years  of  life.  The  Holland  data  make  it  possible  to 
develop  life  tables  for  every  cohort  of  births  and  this 
has  been  done  in  the  16  cohorts  of  males  during  the  years 
1901-1916.  The  data  also  make  it  possible  to  work  up 
these  life  tables  for  urban  areas  and  for  rural  areas. 
After  carefully  eliminating  secular  disturbances  the 
Holland  material  appears  to  prove  quite  conclusively  for 
the  rural  districts  that  there  is  a  definite  negative  corre- 
lation, of  significant  magnitude,  between  infant  mortality 
and  the  mortality  in  the  immediately  subsequent  years  of 
life.  The  only  place  where  positive  correlation  appears  is 
in  the  four  large  cities  of  the  country  -with  more  than  a 
hundred  thousand  inhabitants  each.  Fisher  makes  the 
following  point  (in  a  letter  to  the  present  writer)  in  ex- 
planation of  these  positive  correlations.     He  says  : 

The  larger  cities  are  better  equipped  with  hospital  and  clinical 
facilities  than  the  smaller  cities  and  the  rural  districts.  More  money 
is  also  spent  on  child  welfare.  Is  it  therefore  not  possible  that  many  feeble 
lives  who  in  the  course  of  natural  circumstances  would  have  died  in  the 
first  year  of  life  are  carried  over  into  the  second  year  of  life  by  means 
of  medical   skill?      But   medicine   cannot   always   surpass    nature,   and    it 


THE  INHERITANCE  OF  DURATION         185 

might  indeed  be  possible  that  among  cohorts  with  a  low  mortality  during 
the  first  two  years  of  life  there  will  be  an  increase  of  death  rate  in  the 
following  three  years  of  life. 

Altogether,  we  may  regard  the  weight  of  present  evi- 
dence as  altogether  preponderant  in  favor  of  the  view 
that  the  death  rate  of  the  earliest  period  of  life  is  selec- 
tive— eliminating  the  tveak  and  leaving  the  strong.  From 
our  present  point  of  \dew  it  adds  another  broad  class  of 
evidential  material  to  the  proof  of  the  proposition  that 
inheritance  is  one  of  the  strongest  elements,  if  not  indeed 
the  dominating  factor,  in  determining  the  duration  of 
life  of  human  beings. 


CHAPTER  VII 

EXPERIMENTAL  STUDIES  ON  THE  DURATION 

OF  LIFE 

INHEKITANCE   OF   DUBATION    OF   LIFE   IN   DEOSOPHILA 

In  the  last  chapter  there  was  presented  indubitable 
proof  that  inheritance  is  a  major  factor  in  determining 
the  duration  of  life  in  man.  The  evidence,  while  entirely 
convincing  and  indeed  in  the  writer's  opinion  critically 
conclusive,  must  be,  in  the  nature  of  the  case,  statistical 
in  its  nature.  Experimental  inquiries  into  the  duration 
of  human  life  are  obviously  impossible.  It  is  always 
important,  however,  as  a  general  principle,  and  particu- 
larly so  in  the  present  instance,  to  check  one's  statistical 
conclusions  by  independent  experimental  evidence.  This 
can  be  successfully  done,  when  one's  problem  is  longevity, 
only  by  choosing  an  animal  whose  life-span  relative  to 
that  of  man  is  a  short  one,  and  in  general  the  briefer  it 
is,  the  better  suited  ^vill  the  animal  be  for  the  purpose. 

An  organism  which  rather  completely  fulfils  the  re- 
quirements of  the  case,  not  only  in  respect  of  the  short- 
ness of  the  life  span,  but  also  in  other  ways,  such  as 
ease  of  handling,  feeding,  housing,  etc.,  is  the  common 
''fruit"  or  ''vinegar"  fly,  DrosopMla  melanogaster. 
This  insect,  wliich  every  one  has  seen  hovering  about 
bananas  and  other  fruit  in  fruit  shops,  has  lately  attained 
great  fame  and  respectability  as  a  laboratory  animal, 
as  a  result  of  the  brilliant  and  extended  investigations 
of  Morgan  and  his  students  upon  it,  in  an  analysis  of  the 
mechanism  of  heredity.     DrosopMla  is  a  small  fly,  per- 

186 


STUDIES  ON  THE  DURATION  OF  TJFE      187 


haps  one  fourth  as  large  as  the  common  house  tiy.  It 
has  striking  red  eyes,  a  l)ro\vnish  body,  and  wings  of 
length  and  form  varying  in  different  strains.  It  lives 
normally  on  the  surface  of  decaying  fruit  of  all  sorts, 
but  because  of  a  more  or  less  well-marked  preference  for 


Fig.  46. — Male  and  female  fruit  fly.      {Drosophila  melanogaster).     (From  Morgan). 

banana  it  is  sometimes  called  the  ''banana"  fly.  AVliile 
it  lives  on  decaying  fruit  surfaces  its  food  is  mainly  not 
the  fruit  itself,  but  the  yeast  wliich  is  always  growing 
in  such  places. 

The  life  cycle  of  the  fly  is  as  follows:  The  egg  laid  l)y 
the  female  on  some  fairly  dry  spot  on  the  food  develops 
in  about  1  day  into  a  larva.  Tliis  larva  or  maggot  crawls 
about  and  feeds  in  the  rich  medium  in  which  it  liiids 
itself  for  about  3  to  4  days  and  then  forms  a  pni)a.  From 
the  pupa  the  ^vinged  imago  or  adult  form  emerges  in 
about  4  or  5  days.  The  female  generally  begins  to  lay 
eggs  within  the  first  24  hours  after  she  is  hatched.     So 


188 


BIOLOGY  OF  DEATH 


then  we  have  about  8  to  10  days  as  the  minimum  time 
duration  of  a  generation.  The  whole  cycle  from  egg  to 
egg,  at  ordinary  room  temperature,  falls  mthin  this  10- 
day  period  with  striking  accuracy  and  precision. 

The  duration  of  life  of  the  adult  varies  in  an  orderly 
manner  from  less  than  1  day  to  over  90  days.     The  span 


JOOO 


73 


34 


i>0 


AOL    IN    DAYS 


Fig.  47. — Life  line3  for  Droaophila  m elan og aster;  showing  the  survivors  at  different  agea  out 

of  1000  born  at  the  same  time. 

of  life  of  Drosophila  quantitatively  parallels  in  an  extra- 
ordinary way  that  of  man,  mth  onl}^  the  difference  that 
life's  duration  is  measured  with  different  yardsticks  in 
the  two  cases.  Man's  yardstick  is  one  year  long,  while 
DrosopJiila's  is  one  day  long.  A  fly  90  days  old  is  just 
as  decrepit  and  senile,  for  a  fly,  as  a  man  90  years  old 
is  in  human  society. 

This  parallelism  in  the  duration  of  life  of  Drosophila 
and  man  is  well  shown  in  Figure  47,  which  represents  a 
life  table  for  adult  flies  of  both  sexes.  The  survivor- 
ship, or  Ix  figures,  are  the  ones  plotted.     The  curves  deal 


STUDIES  ON  THE  DURATION  OF  LIFE      180 

only  with  flies  in  the  adult  or  imago  stage,  after  the  com- 
pletion of  the  larval  and  pupal  periods.  The  curve  is 
based  upon  3,216  female  and  2,620  male  flies,  large  enough 
numbers  to  give  reliable  and  smooth  results.  We  note  at 
once  that  in  general  the  curve  has  the  same  form  as  the 
corresponding  h  curve  from  human  mortality  tables.  The 
most  striking  difference  is  in  the  absence  from  the  fly 
curves  of  the  heavy  infant  mortality  which  characterizes 
the  human  curve.  There  is  no  specially  sharp  drop  in  the 
curve  at  the  beginning  of  the  life  cycle,  such  as  has  been 
seen  in  the  h  curve  for  man  in  an  earlier  chapter  in  this 
book.  This  might  at  first  be  thought  to  be  accounted 
for  by  the  fact  that  the  curve  begins  after  the  infantile  life 
of  the  fly,  but  it  must  be  remembered  that  the  human  I  z 
line  begins  at  birth,  and  no  account  is  taken  of  the  mortal- 
ity in  utero.  Really  the  larval  and  pupal  stages  of  the 
fly  correspond  rather  to  the  foetal  life  of  a  human  being 
than  to  the  infant  life,  so  that  one  may  perhaps  fairly  take 
the  curves  as  covering  comparable  portions  of  the  life  span 
in  the  two  cases  and  reach  the  conclusion  that  there  is  not 
in  the  fly  an  especially  heavy  incidence  of  mortality  in 
the  infant  period  of  life,  as  there  is  in  man.  The  explana- 
tion of  this  fact  is,  mthout  doubt,  that  the  fly  when  it 
emerges  from  the  pupal  stage  is  completely  able  to  take 
care  of  itself.  The  baby  is,  on  the  contrary,  in  an  almost 
totally  helpless  condition  at  the  same  relative  age. 

It  is  further  evident  that  at  practically  all  ages  in 
Drosophila  the  number  of  survivors  at  any  given  age 
is  higher  among  the  female  than  among  the  males.  This, 
it  will  be  recalled,  is  exactlv  the  state  of  the  case  in  human 
mortality.  The  speed  of  the  descent  of  the  Drosophila 
curve  slows  off  in  old  age,  just  as  happens  in  the  human 
life  curve.  The  rate  of  descent  of  the  curve  in  early 
middle  life  is  somewhat  more  rapid  with  the  flies  than 


190  BIOLOGY  OF  DEATH 

in  the  case  of  human  beings,  but  as  will  presently  appear 
there  are  some  strains  of  flies  which  give  curves  almost 
identical  in  this  respect  with  the  human  mortality  curves. 
In  the  life  curves  of  Figure  47,  all  different  degrees  of 
inherited  or  constitutional  variation  in  longevity  are  in- 
cluded together.  More  accurate  pictures  of  the  true  state 
of  affairs  will  appear  when  we  come,  as  we  presently 
shall,  to  deal  with  groups  of  individuals  more  homoge- 
neous in  respect  of  their  hereditary  constituents. 

Having  now  demonstrated  that  the  incidence  of  mor- 
tality is  in  general  similar  in  the  fly  Drosophila  to  what 
it  is  in  man,  with  a  suitable  change  of  unit  of  measure, 
we  may  proceed  to  examine  some  of  the  evidence  regarding 
the  inheritance  of  duration  of  life  in  this  organism. 
The  first  step  in  such  an  examination  is  to  determine 
what  degree  of  natural  variation  of  an  hereditary 
sort  exists  in  a  general  fly  population  in  respect  of  this 
characteristic.  In  order  to  do  this  it  is  necessary  to 
isolate  individual  pairs,  male  and  female,  breed  them 
together  and  see  whether,  between  the  groups  of  offspring 
so  obtained,  there  are  genetic  differences  in  respect  of 
duration  of  life  which  persist  through  an  indefinite  num- 
ber of  generations.  This  approaches  closely  to  the  pro- 
cess called  by  geneticists  the  testing  of  pure  lines.  In 
such  a  process  the  purpose  is  to  reduce  to  a  minimum 
the  genetic  diversity  which  can  possibly  be  exhibited  in 
the  material.  In  a  case  like  the  present,  the  whole  amount 
of  genetic  variation  in  respect  of  duration  of  life  which  can 
appear  in  the  offspring  of  a  single  pair  of  parents  is  only 
that  which  can  arise  by  virtue  of  its  prior  existence  in  the 
parents  themselves  indi\^dually,  and  from  the  combina- 
tion of  the  germinal  variation  existing  in  the  two  parents 
one  with  another.  We  may  call  the  offspring,  through 
successive  generations,  of  a  single  pair  of  parents  a  line 


STUDIES  ON  THE  DURATION  OF  LIFE      191 

of  descent.  If,  when  kept  under  identical  environmental 
conditions,  such  lines  exhibit  widely  different  average 
durations  of  life,  and  if  these  differences  reappear  witli 
constancy  in  successive  generations,  it  may  be  justly 
concluded  that  the  basis  of  these  diiTerences  is  heredi- 
tary in  nature,  since  by  hypothesis  the  environment  of 
all  the  lines  is  kept  the  same.  In  consequence  of  the 
environmental  equality,  whatever  differences  do  api)ear 
must  be  inherently  genetic. 

The  manner  in  wliich  these  experiments  are  performed 
may  be  of  interest.     An  experiment  starts  by  i)lacing 
two  flies,  brother  and  sister,  selected  from  a  stock  bottle, 
together  in  a  half -pint  milk  bottle.     At  the  bottom  of  the 
bottle  is  a  solidified,  jelly-like  mixture  of  agar-agar  and 
boiled  and  pulped  banana.     On  this  is  sown,  as  food,  some 
dry  yeast.     A  bit  of  folded  filter  paper  in  the  bottle  fur- 
nishes the  larvae  opportunity  to  pupate  on  a  dry  sur- 
face.    About  ten  days  after  the  pair  of  flies  have  been 
placed  in  this  bottle,  fully  developed  offspring:  in  tlie 
imago  stage  begin  to  emerge.     The  day  before  these  olY- 
spring  flies  are  due  to  appear,  the  original  parent  pair 
of  flies  are  removed  to  another  bottle  precisely  like  the 
first,  and  the  female  is  allowed  to  lay  another  batch  of 
eggs  over  a  period  of  about  nine  days.     In  the  original 
bottle  there  will  be  offspring  flies  emerging  each  day, 
having  developed  from  the  eggs  laid  by  tlie  mother  on 
each  of  the  successive  days  during  wliieli  she  was  in  the 
bottle.     Each  morning  the   offspring  flies    which    have 
emerged   during  the   preceding   twenty-four   hours   are 
transferred   to   a   small   bottle.     This  has,   just   as   the 
larger  one,  food  material  at  the  bottom  and  like  the  larger 
one  is  closed  with  a  cotton  stopper.     All  of  the  offs])ring 
flies  in  one  of  these  small  bottles  are  obviously  of  the 
same  age,  because   they  were  born   at  tlie   same   time, 


192 


BIOLOGY  OF  DEATH 


using  this  term  ''born''  to  denote  emergence  from  the 
pupal  stage  as  imagines.  Each  following  day  these  small 
bottles  are  inspected.  Whenever  a  dead  fly  is  found,  it 
is  removed  and  a  record  made  in  proper  form  of  the 
fact  that  its  death  occurred,  and  its  age  and  sex  are  noted. 
Finally,  when  all  the  flies  in  a  given  small  bottle  have 
died,  that  bottle  is  discarded,  as  the  record  of  the  duration 


1,000 


30         36         42.         4b  5A         60         66         7^  IQ         eA         90 


AGE.     IN   DAYS 

Fig.  48. — Life  lines  for  different  inbred  lines  of  descent  in  Drosophila. 

of  life  of  each  individual  is  then  complete.  All  the 
bottles  are  kept  in  electric  incubators  at  a  constant 
temperature  of  25°  C,  the  small  bottles  being  packed  for 
convenience  in  wire  baskets.  All  have  the  same  food 
material,  both  in  quality  and  quantity,  so  that  the  envi- 
ronmental conditions  surrounding  these  flies  during  their 
life  may  be  regarded  as  substantially  constant  and  uni- 
form for  all. 

Figure  48  shows  the  survival  frequency,  or  Ix  line 
of  a  life  table,  for  six  different  lines  of  Drosophila,  which 
have  been  bred  in  my  laboratory.     Each  line  represents 


' 


STUDIES  ON  THE  DURxVTION  OF  LIFE      193 

the  survival  distribution  of  the  olTspring  of  a  single 
brother  and  sister  pair  mated  together.  In  forming  a 
line  a  brother  and  sister  are  taken  as  the  initial  start 
because  by  so  doing  the  amount  of  genetic  variation  pres- 
ent in  the  line  at  the  beginning  is  reduced  to  the  lowest 
possible  minimum.  It  should  be  said  that  in  all  of  the 
curves  in  Figure  48,  both  male  and  female  olfspring  are 
lumped  together.  This  is  justifiable  for  illustrative  pur- 
poses because  of  the  small  difference  in  the  expectation 
of  life  at  any  age  between  the  sexes.  The  line  of  descent, 
No.  55,  figured  at  the  top  of  the  diagram,  gives  an  I  z 
line  extraordinarily  like  that  for  man,  with  the  exception 
of  the  omission  of  the  sharp  drop  due  to  infantile  mor- 
tality at  the  beginning  of  the  curve.  The  extreme  dura- 
tion of  life  in  this  line  was  81  days,  reached  by  a  female 
fly.  The  U  line  drops  off  very  slowly  until  age  36  days. 
Prom  that  time  on,  the  descent  is  more  rapid  until  72  days 
of  age  are  reached  when  it  slows  up  again.  Lines  50,  60, 
and  58  show  h  curves  all  descending  more  rapidly  in  the 
early  part  of  the  life  cycle  than  that  for  line  55,  although 
the  maximum  degree  of  longevity  attained  is  about  the 
same  in  all  of  the  four  first  curves.  The  general  shape 
of  the  Ix  curves  changes  however,  as  is  clearly  seen  if 
we  contrast  line  55  with  line  58.  The  former  is  concave 
to  the  base  through  nearly  the  whole  of  its  course,  whereas 
the  Ix  curve  for  line  58  is  convex  to  the  base  practically 
throughout  its  course.  While,  as  is  clear  from  the  dia- 
gram, the  maximum  longevity  attained  is  about  the  same 
for  all  of  these  upper  four  lines,  it  is  equally  ob\'ious 
that  the  mean  duration  of  life  exliibited  by  the  lines  falls 
off  as  we  go  down  the  diagram.  The  same  process,  which 
is  in  operation  between  lines  55  and  58,  is  continued  in 
an  even  more  marked  degree  in  lines  61  and  64.  Here 
not  only  is  the  descent  more  rapid  in  the  early  part  of  the 

13 


194  BIOLOGY  OF  DEATH 

Ix  curve,  but  the  maximum  degree  of  longevity  attained 
is  much  smaller,  amounting  to  about  half  of  that  attained 
in  the  other  four  lines.  Both  lines  61  and  64  tend  to  show 
in  general  a  curve  convex  to  the  base,  especially  in  the 
latter  half  of  their  course. 

Since  each  of  these  lines  of  descent  continues  to  show 
through  successive  generations,  for  an  indefinite  time, 
the  same  types  of  mortality  curves  and  approximately 
the  same  average  durations  of  life,  it  may  safely  be  con- 
cluded that  there  are  well  marked  hereditary  differences 
in  different  strains  of  the  same  species  of  Drosophila  in 
respect  of  duration  of  life.  Passing  from  the  top  to  the 
bottom  of  the  diagram  the  average  expectation  of  life  is 
reduced  by  about  two-thirds  in  these  representative 
curves.  For  purposes  of  experimentation,  each  one  of 
these  lines  of  descent  becomes  comparable  to  a  chemical 
reagent.  They  have  standard  durations  of  life,  each 
peculiar  to  its  o^vn  line  and  determined  by  the  hereditary 
constitution  of  the  individual  in  respect  of  this  charac- 
ter. We  may,  with  entire  justification,  speak  of  the 
flies  of  line  64  as  hereditarily  short-lived,  and  those  of 
line  55  as  hereditarily  long-lived. 

Having  established  so  much,  the  next  step  in  the  analy- 
sis of  the  mode  of  inheritance  of  tliis  character  is  ob- 
viously to  perform  a  Mendelian  experiment  by  crossing 
an  hereditarily  short-lived  line  with  an  hereditarily  long- 
lived  line,  and  follow  through  in  the  progeny  of  succes- 
sive generations  the  duration  of  life.  If  the  character 
follows  the  ordinary  course  of  Mendelian  inheritance,  we 
should  expect  to  get  in  the  second  offspring  generation  a 
segregation  of  different  types  of  flies  in  respect  of  their 
duration  of  life. 

Fig-ure  49  shows  the  result  of  such  Mendelian  experi- 


STUDIES  ON  THE  DURATION  OF  LIFE      195 

ment  performed  on  a  large  scale.  In  the  second  line  from 
the  top  of  the  diagram,  labeled  ^'Type  I  /.,"  we  see  the 
mortality  curve  for  an  hereditarily  long-lived  pure  strain 
of  individuals.  At  thebottom  of  the  diagram  the'^Type  1 V 
Ix  ''  line  gives  the  mortality  curve  for  one  of  our  heredita- 
rily short-lived  strains.  Individuals  of  Typel  andTvpoIV 


LOOO 


It  13  c-^  30         JO  -4J         ^  S4  to         C6 


e-i      M 


•  AGL  IN    DAVa 

Fia.  49. — Life  lines  showing  the  result  of  Mendelian  experiments  on  the  duration  of  life  in 

Drosophila.    Explanation  in  text. 

were  mated  together.  The  result  in  the  first  oiTspring 
hybrid  generation  is  shown  by  the  line  at  the  top  of  dia- 
gram marked  ^  ^  Fj  Za;."  The Fi denotes  that  this  is  the  mor- 
tality curve  of  the  first  filial  generation  from  the  cross. 
It  is  at  once  obvious  that  these  first  generation  hybrids 
have  a  greater  expectation  of  life  at  practically  all  ages 
than  do  either  of  the  parent  strains  mated  togetluM'  to 
produce  the  hybrids.  The  result  is  exactly  comparable 
to  that  which  has  for  some  time  been  known  to  oc^'ur 
in  plants,  from  the  researches  particularly  of  Piast  and 
others  with  maize.     East  and  his  students  have  worked 


196  BIOLOGY  OF  DEATH 

out  very  thoroughly  the  cause  of  this  increased  vigor  of 
the  first  hybrid  generation  and  show  that  it  is  directly 
due  to  the  mingling  of  different  germ  plasms. 

The  average  duration  of  life  of  the  Type  I  original 
parent  stock  is  44.2  ±  .4  days.  The  average  duration  of 
life  of  the  short-lived  Type  IV  flies  is  14.1  ±  .2  days,  or 
only  about  one  third  as  great  as  that  of  the  other  stock. 
The  average  duration  of  life  of  the  first  hybrid  genera- 
tion shown  in  the  Fj  h  line  is  51.5  ±  .5  days.  So  that 
there  is  an  increase  in  average  duration  of  life  in  the 
first  hybrid  generation,  over  that  of  the  long-lived  parent, 
of  approximately  7  days.  In  estimating  the  significance 
of  this,  one  should  remember  that  a  day  in  the  life  of  a 
fly  corresponds,  as  has  already  been  pointed  out,  almost 
exactlv  to  a  vear  in  the  life  of  a  man. 

When  individuals  of  the  first  hybrid  generation  are 
mated  together  to  get  the  second,  or  Fg  hybrid  generation 
we  get  a  group  of  flies  which,  if  taken  all  together,  give 
the  mortality  curve  shown  in  the  line  at  about  the  middle 
of  the  diagram,  labelled  ^'All  F2  /:r."  It,  however,  tells 
us  little  about  the  mode  of  inheritance  of  the  character 
if  we  consider  all  the  individuals  of  the  second  hybrid 
generation  together,  because  really  there  are  several 
kinds  of  flies  present  in  this  second  hybrid  generation. 
There  are  sharply  separated  groups  of  long-lived  flies  and 
of  short-lived  flies.  These  have  been  lumped  together  to 
give  the  ''All  F2  ?;r"  line.  If  we  consider  separately  the 
long-lived  second  generation  group  and  the  short-lived 
second  generation  group  we  get  the  results  shown  in  the 
two  lines  labelled  ''Long-lived  F^  Segregates  h,''  and 
"Short-lived  F2  Segregates  L .''  It  will  be  noted  that  the 
long-lived  Fg  segregates  have  a  mortality  curve  which  al- 
most exactly  coincides  with  that  of  the  original  parent  Type 
I  stock.     In  other  words,  in  the  second  generation  after 


STUDIES  ON  THE  DURATION  OF  LIFE      197 

the  cross  of  the  long-lived  and  short-lived  types,  a  group 
of  animals  appears  having  almost  identically  the  same 
form  of  mortality  curve  as  that  of  one  of  the  original 
parents  in  the  cross.  The  mean  duration  of  life  of  this 
long-lived  second  generation  group  is  43.3  ±  .4  days, 
while  that  of  the  original  long-lived  stock  was  44.2  ±  -4 
days.  The  short-lived  Fo  segregates,  sho^\^l  at  the  bottom 
of  the  diagram,  give  a  mortality  curve  essentially  like 
that  of  the  original  short-lived  parent  strain.  The  two 
curves  wind  in  and  about  each  other,  the  F^  flies  showing 
a  more  rapid  descent  in  the  first  half  of  the  curve  and  a 
slower  descent  in  the  latter  half.  In  general,  however, 
the  two  are  very  clearly  of  the  same  form.  The  aver- 
age duration  of  life  of  these  short-lived  second  generation 
segregates  is  14.6  db  .6  days.  Tliis,  it  will  be  recalled, 
is  almost  identically  the  same  average  duration  of  life 
as  the  original  parent  Type  IV  gave,  which  was  14.1  ± 
.2  days. 

It  may  occur  to  one  to  wonder  how  it  is  possible  to 
pick  out  the  long-lived  and  short-lived  segregates  in  the 
second  generation.  This  is  done  by  virtue  of  the  corre- 
lation of  the  duration  of  life  of  these  flies  with  certain 
external  bodily  characters,  particularly  the  form  of 
the  wings,  so  that  this  arrangement  of  the  material  can 
be  made  with  perfect  ease  and  certainty. 

These  results  show  in  a  clear  manner  that  duration  of 
life,  in  Drosophila  at  least,  is  inherited  essentially  in 
accordance  with  Mendelian  laws,  thus  fitting  in  with  a 
wide  range  of  other  physical  characters  of  the  animal 
which  have  been  thoroughly  studied  particularly  by 
Morgan  and  his  students.  Such  results  as  these  just 
showm  constitute  the  best  kind  of  proof  of  the  essential 
point  which  we  are  examining — namely,   the   fact  that 


198  BIOLOGY  OF  DEATH 

duration  of  life  is  a  normally  inherited  character.  I  do 
not  wish  at  tliis  time  to  go  into  any  discussion  of  the 
details  of  the  Mendelian  mechanism  for  this  character, 
in  the  first  place,  because  it  is  too  complicated  and  tech- 
nical a  matter  for  discussion  here*  and,  in  the  second 
place,  because  the  investigations  are  far  from  being  com- 
pleted yet.  I  wish  here  and  now  merely  to  present  the 
demonstration  of  the  broad  general  fact  that  duration 
of  life  is  inherited  in  a  normal  Mendelian  manner  in 
these  fly  populations.  The  first  evidence  that  this  was 
the  case  came  from  some  work  of  Dr.  R.  R.  Hyde  with 
Drosophila  some  years  ago.  The  numbers  involved  in 
his  experiment,  however,  were  much  smaller  than  those 
of  the  present  experiments,  and  the  preliminary  demon- 
stration of  the  existence  of  pure  strains  relative  to  dura- 
tion of  life  in  Drosophila  was  not  undertaken  by  him. 
Hyde's  results  and  those  here  presented  are  entirely 
in  accord. 

With  the  evidence  wliich  has  now  been  presented  re- 
garding the  inheritance  of  life  in  man  and  in  Drosophila 
we  may  let  that  phase  of  the  subject  rest.  The  evidence 
is  conclusive  of  the  broad  fact,  beyond  any  question  I 
think,  coming  as  it  does  from  such  widely  different  types 
of  life,  and  arrived  at  by  such  totally  different  methods  as 
the  statistical,  on  the  one  hand,  and  the  experimental,  on 
the  other.  We  may  safely  conclude  that  the  primary  agent 
concerned  in  the  mnding  up  of  the  \dtal  clock,  and  by 
the  mnding  determining  primarily  and  fundamentally 
how  long  it  shall  run,  is  heredity.  The  best  insurance 
of  longevity  is  beyond  question  a  careful  selection  of 
one's  parents  and  grandparents. 

*  Full  technical  details  and  all  the  numerical  data  regarding  these  and 
other  Drosophila  experiments  referred  to  in  this  book  will  shortly  be 
published  elsewhere. 


STUDIES  ON  THE  DURATION  OF  LIFE      199 

BACTERIA   AND   DURATION    OF   LIFE    IN    DROSOPHILA 

But  clocks  may  be  stopped  in  otiier  ways  tlian  by 
nmning  do^\^l.  It  will  be  worth  while  to  consider  witii 
some  care  a  considerable  mass  of  most  interesting,  and 
in  some  respects  even  startling,  experimental  data,  re- 
garding various  ways  in  which  longevity  may  be  influenced 
by  external  agents.  Since  Ave  have  just  been  considering 
Drosophila  it  may  be  ^vell  to  consider  the  experimental 
evidence  regarding  that  form  first.  It  is  an  obviously 
well-known  fact  that  bacteria  are  responsible  in  all  higher 
organisms  for  much  organ  breakdown  and  consequent 
death.  An  infection  of  some  particular  organ  or  organ 
system  occurs,  and  the  disturbance  of  the  balance  of  the 
whole  so  brought  about  finally  results  in  death.  But  is 
it  not  possible  that  we  overrate  the  importance  of  bacter- 
ial invasion  in  determining,  in  general  and  in  the  broad- 
est sense,  the  average  duration  of  life?  May  it  not  be 
that  when  an  organ  system  breaks  do^vn  under  stress 
of  bacterial  toxins,  it  is  in  part  at  least,  perhaps 
primarily,  because  for  internal  organic  reasons  the  resis- 
tance of  that  organ  system  to  bacterial  invasion  has  nor- 
mally and  naturally  reached  such  a  low  ])oint  that  its 
defenses  are  no  longer  adequate?  All  higher  animals 
live  constantly  in  an  environment  far  from  sterile.  Our 
mouths  and  throats  harbor  pneumonia  germs  much  of 
the  time,  but  w^e  do  not  all  or  always  have  pneumonia. 
Again  it  may  fairly  be  estimated  that  of  all  persons  who 
attain  the  age  of  35,  probably  at  least  95  per  cent,  have 
at  some  time  or  other  been  infected  with  the  tubercle 
bacillus,  yet  fewer  than  one  in  ten  break  downi  with 
active  tuberculosis. 

What  plainly  is  needed  in  order  to  arrive  at  a  just 
estimate  of  the  relative  influence  of  bacteria  and  their 


200  BIOLOGY  OF  DEATH 

toxins  in  determining  the  average  duration  of  life  is  an 
experimental  inquiry  into  the  effect  of  a  bacteria-free, 
sterile  mode  of  life.  Metchnikoif  has  sturdily  advocated 
the  view  that  death  in  general  is  a  result  of  bacterial 
intoxication.  Now  a  bacteria-free  existence  is  not  pos- 
sible for  man.  But  it  is  possible  for  certain  insects, 
as  was  first  demonstrated  by  Bogdanow,  and  later  con- 
firmed by  Delcourt  and  Guyenot.  If  one  carefully  washes 
either  the  egg  or  the  pupa  of  DrosopMla  for  10  minutes 
in  a  strong  antiseptic  solution,  say  85  per  cent,  alcohol, 
he  will  kill  any  germ  which  may  be  upon  the  surface.  If 
the  bacteria-free  egg  or  pupa  is  then  put  into  a  sterile 
receptacle,  containing  only  sterile  food  material  and  a 
pure  culture  of  yeast,  development  will  occur  and  pre- 
sently an  adult  imago  will  emerge.  Adult  flies  raised  in 
this  way  are  sterile.  They  have  no  bacteria  inside  or 
out.  Normal  healthy  protoplasm  is  normally  sterile,  so 
what  is  inside  the  fly  is  bound  to  be  sterile  on  that  account, 
and  by  the  use  of  the  antiseptic  solution  what  bacteria 
were  on  the  outside  have  been  killed. 

The  problem  now  is,  how  long  on  the  average  do  such 
sterile  specimens  of  Drosophila  live  in  comparison  vnih. 
the  ordinary  fly,  which  is  throughout  its  adult  life  as 
much  beset  by  bacteria  relatively  as  is  man  himself,  it 
being  premised  that  in  both  cases  an  abundance  of  prop- 
er food  is  furnished  and  that  in  general  the  environ- 
mental conditions,  other  than  bacterial,  are  made  the  same 
for  the  two  sets?  Fortunately,  there  are  some  data  to 
throw  light  upon  this  question  from  the  experiments  of 
Loeb  and  his  associate  Northrop  on  the  duration  of  life 
in  this  form,  taken  in  connection  mth  experiments  in  the 
writer's  laboratory. 

Loeb  and  Northrop  show  that  a  sample  of  70  flies,  of 
the   Drosophila  with  which  they  worked,   which  were 


STUDIES  ON  THE  DURATION  OF  LIFE     201 

proved  by  the  most  careful  and  critical  of  tests  to  have 
remained  entirely  free  of  bacterial  contamination  through- 
out their  lives,  exhibited,  when  gro^^^l  at  a  constant  tem- 
perature of  25°  C.  an  average  duration  of  life  of  28.5 
days.  In  our  experiments  2,620  male  flies,  of  all  strains 
of  Drosophila  in  our  cultures  taken  together,  thus  giv- 
ing a  fair  random  sample  of  genetically  the  whole  Droso- 
pliila  population,  gave  an  average  duration  of  life  at  the 
same  constant  temperature  of  25"^  C.  of  31.3  ±.3  days, 
and  3,216  females  under  the  same  temperature  lived  an 
average  of  33.0  =i=  .2  days  These  were  all  non-sterile 
flies,  subject  to  all  the  bacterial  contamination  incident 
to  their  normal  laboratory  environment,  which  we  have 
seen  to  be  a  decaying  germ-laden  mass  of  banana  pulp  and 
agar.  It  is  thought  to  be  fairer  to  compare  a  sample  of 
a  general  population  w^ith  the  Loeb  and  Northrop  figures 
rather  than  a  pure  strain  because  probably  their  Droso- 
phila material  was  far  from  homozygous  in  respect  of 
the  genes  for  duration  of  life. 

The  detailed  comparisons  are  sho^^^l  in  Table  23. 

TABLE  23 

Average  duration  of  life  of  Drosophila  in  the  imago  stage  at  26^  C. 


Experimental  group 

Mean  duration 
of  life  iu  days 

Number  of 
(lies) 

Sterile  (Loeb  and  Northrop) 

28.5 
31.3 
33.0 
32.2 

70 

Non-sterile,      males,      all  genetic  lines  (Pearl) 
Non-sterile,     females,     all  genetic  lines  (Pearl) 
Non-sterile,  both  sexes,  all  genetic  lines  (Pearl) 

2(:)20 
3210 
5830 

Difference  in  favor  of  non-sterile 

Probable  error  of  difference  about 

3.7 
±  1.0 

We  reach  the  conclusion  that  bacteria-free  Drosophila 
live  no  longer  on  the  average,  and  indeed  perhaps  even 
a  little  less  long,  under  otherwise  the  same  constant 


202 


BIOLOGY  OF  DEATH 


environmental  conditions,  than  do  normal  non-sterile — 
indeed  germ-laden — flies.  This  result  is  of  great  inter- 
est and  significance.  It  emphasizes  in  a  direct  experi- 
mental manner  that  in  a  broad  biological  sense  bacteria 
play  but  an  essentially  accidental  role  in  determining 
length  of  the  span  of  life  in  comparison  with  the  influence 
of  heredity. 

POVERTY  AND  DURATION  OF  LIFE 

But  we  must  take  care  lest  we  seem  to  convey  the 
impression  that  no  sort  of  environmental  influence  can 
affect  the  average  duration  of  life.  Such  a  conclusion 
would  be  manifestly  absurd.     Common  sense  tells  us 


PERSONAL      PROPERTY 

1        I   RAYING 


TAX     IN     PARIS 


1911  -  )9I3 


i 


fe 


€    16    9       Tine       10    2    3     5    4    IZ    14    15   18    II 
ARF0NDIS5LMLNTS 


13    19  ZO 


I       n      ffl      17 

CLAS5LS    OF 
/^RmaSSD€MTS 


PARIS 


Fig.  50. — Distribution  of  poverty  in  Paris  (1911-13)  as  indicated  by  exemption  from  personal 

property  tax.     (After  Hersch). 

that  environmental  conditions  in  general  can,  and  under 
some  circumstances,  do  exert  a  marked  influence  upon 
expectation  of  life.  A  recent  study  of  great  interest  and 
suggestiveness,  if  perhaps  some  lack  of  critical  sound- 
ness, by  the  eminent  Swiss  statistician,  Hersch,  may 
be  cited  in  this  comiection.  Hersch  became  interested 
in  the  relation  of  poverty  to  mortality.     He  gathered 


STUDIES  ON  THP]  DURATION  OF  LIFE     203 


data  from  the  20  arrondisscmonts  of  tho  citv  of  Paris  in 
respect  of  the  following  points,  amoni»;  others: 

a.  Percentage  of  families  not  paying  a  personal  property  tar. 

b.  Death  rate  per  1000  from  all  causes. 

c.  Stillbirths  per  1000  living  ])irths. 

Figure  50  shows  in  the  black  the  percentage  of  fam- 
ilies too  poor  to  have  any  personal  property  tax  assessed, 
first  for  each  arrondissement  separately,   then  at  the 

MORTAUTY      IN       PARIS        1911  ■  I9l3 


6     9    16        ,     7     17    6       Z    iO    3    IS    IZ    4     5    ,1    15    ^       l9  20  13  '^^^5^^" 

ARRONDlSSCMDfrS  /mmSSCMCNTS 

Fio.  51. — Death  rates  in  Paris  (1911-13)  from  all  causes.     (After  Hersch). 

right  in  broader  bars  for  the  four  groups  of  arrondisse- 
ments  separated  by  wider  spaces  in  the  detailed  dia- 
gram, and  finally  for  Paris  as  a  whole.  It  will  be  seen 
that  the  poverty  of  the  population,  measured  by  the  per- 
sonal property  yardstick,  is  least  at  the  left-hand  end  of 
the  diagram,  where  the  smallest  percentages  of  fam- 
ilies are  exempted  from  the  tax,  and  greatest  at  the 
right-hand  end,  where  scarcely  any  of  the  ])(>pnhi(i()n  is 
well  enough  to  do  to  pay  this  tax. 

Figure  51  shows  the  death  rates  from  all  causes  t'(»r 
the  same  arrondissements  and  the  same  groups.  It  is 
at  once  apparent  that  the  black  bars  in  this  group  run  in 
a  general  manner  parallel   to  the  preceding  one.     Tlie 


204  BIOLOGY  OF  DEATH 

poorest  districts  have  the  highest  death  rates,  the  richest 
districts  the  lo,west  death  rates,  and  districts  interme- 
diate in  respect  of  poverty  are  also  intermediate  in  res- 
pect of  mortality.  On  the  face  of  the  evidence  there 
would  seem  to  be  here  complete  proof  of  the  overwhelm- 
ingly important  influence  upon  duration  of  life  of  degree 
of  poverty,  which  is  perhaps  the  most  potent  single  envi- 
ronmental factor  affecting  civilized  man  to-day.  But, 
alas,  pitfalls  proverbially  lurk  in  statistics.  Before  we 
can  accept  this  so  alluring  result  and  go  along  with  our 
author  to  his  final  somewhat  stupendous  conclusion  that 
if  there  were  no  poverty  the  death  rate  from  certain  im- 
portant causes,  as  for  example  tuberculosis,  would  forth- 
with become  zero,  we  must  exercise  a  little  inquisitive 
caution.  What  evidence  is  there  that  the  inhabitants  of 
the  districts  shoAving  a  high  poverty  rate  are  not  biologi- 
cally as  well  as  economically  differentiated  from  the  in- 
habitants of  districts  with  a  low  poverty  rate?  And 
again  what  is  the  evidence  that  it  is  not  such  biological 
differentiation  rather  than  the  economic  which  determines 
the  death  rate  differences  in  the  two  cases  ?  Unfortunately, 
our  author  gives  us  no  wliit  of  evidence  on  these  obviously 
so  important  points.  He  merely  assumes,  because  of  the 
facts  shown,  that  if  some  omnipotent  spook  were  to  trans- 
pose all  the  inhabitants  of  the  Menilmontant  arrondisse- 
ment  to  the  Elvsee  arrondissement,  and  vice  versa  for 
example,  and  were  to  permit  each  group  to  annex  the 
worldly  goods  of  the  dispossessed  group,  then  the  death 
rates  would  be  forthwith  interchanged.  There  is  no  real 
evidence  that  any  such  result  would  follow  at  all.  One 
cannot  shake  in  the  slightest  degree  from  its  solidly 
grounded  foundation  the  critically  determined  fact  of 
the  paramount  importance  of  the  hereditary  factor  in 
determining  rates  of  mortality,  which  have  been  summa- 


STUDIES  ON  THE  DURATION  OF  LIFE     205 

rized  in  this  and  the  preceding  chapter  by  any  snch  e\i- 
dence  as  that  of  Hersch. 

TABLE  24 

Stillbirths  in  Paris  (1911-13)  by  classes  of  arrondissemenU  {Hersch) 


Classes  of  Arrondissementa 

Absolute  figures 

Stillbirtha 

per  100  living 

births 

Stillbirths 

Living  births 

I 

II 
III 

IV 

1,004 
1,390 
7,279 
3,024 

12,313 
19,998 
82,821 
30,853 

8.2 
7.0 
8.8 
9.8 

Paris 

12,679 

145,985 

8.7 

This,  indeed,  he  himself  finds  to  be  the  fact  when  he 
considers  the  extremely  sensitive  index  of  hereditary 
biological  constitution  furnished  by  the  still])irth  rate. 
Table  24  gives  the  data.  We  see  at  once  that  there  is  no 
such  striking  increase  in  the  foetal  mortality  as  we  pass 
from  the  richest  class  of  districts,  as  was  shown  in  the 
death  rate  from  all  causes.  Instead  there  is  practically 
no  change,  certainly  none  of  significance,  as  we  pass 
from  one  class  of  districts  to  another.  The  rate  is  8.2 
per  100  living  births  in  the  richest  class  and  9.8  in 
the  poorest. 

Other  definite  evidence  that  such  conclusion  as  those 
of  Hersch  cannot  be  accepted  at  anything  like  their  face 
value  is  afforded  by  the  work  of  Greenwood  and  Bro\m 
on  the  relation  of  poverty  and  the  infant  death  rate. 
They  find,  giving  subscripts  the  following  meanings: 

Subscript  1  =  Birth  rate 
Subscript  2  =  Artificial  feeding  rate 
Subscript  3  =  Poverty  rate 
■  Subscript  4  ^  Infant  death  rate 

that 

r34.i2-=.17±  .07 

on  the  basis  of  the  Bavarian  data  of  Groth  and  Ilalin. 


206  BIOLOGY  OF  DEATH 

Now  this  is  a  statistically  insignificant  net  correlation, 
being  less  even  than  3  times  its  probable  error.  It  means 
that,  when  the  birth  rate  and  artificial  feeding  rate  are 
held  constant,  differences  in  the  infant  death  rate  are 
not  sufficiently  influenced  or  determined  by  differences 
in  the  poverty  rate  to  lead  to  a  coefficient  of  correlation 
significantly  different  from  zero,  so  far  as  Bavarian 
populations  are  indicative. 

This  result  is  further  confirmed  by  an  analysis  which 
Greenwood  and  Bro^\ai  made  of  Heron's  London  mate- 
rial, showing  that  in  that  case 

r34.i  =  .19±  .13 

This  coefficient  means  that  the  differences  in  infant 
mortality  rate  in  the  different  districts  of  London,  when 
the  birth  rate  is  made  constant,  are  not  associated  with 
differences  in  poverty  between  the  same  districts  to  an 
extent  sufficient  to  lead  to  a  correlation  coefficient  sensi- 
blv  different  from  zero. 

Finally,  Stevenson  has,  since  the  appearance  of 
Hersch's  paper,  studied  the  same  problems  on  the  basis 
of  the  London  data,  for  the  sake  of  comparison  with 
the  results  from  Paris.  He  takes  as  the  index  of  eco- 
nomic status  the  number  of  domestic  servants  (of  both 
sexes)  per  100  of  population,  and  has  examined  the  death 
rates  from  all  causes,  infant  mortality,  and  tuberculosis 
for  the  identical  vears  that  Hersch  used.  The  results 
are  set  forth  in  Table  24a. 

Commenting  on  the  facts  regarding  general  mortality 
from  all  causes  in  London,  Stevenson  says: 

"These  bear  an  altofrether  different  aspect  from  the  Parisian  ficrnres. 
Whereas  the  latter  increase  so  re<?ularly  with  poverty  that  the  highest 
rate  for  any  district  in  one  group  never  exceeds  the  lowest  for  any  district 
in  the  next  poorer  group,  in  London  the  gradation,  even  for  the  groups 
themselves,  is  irregular,  the  lowest  death-rate  not  being  returned  for  the 


STUDIES  ON  THE  DURATION  OF  LIFE     207 

TABLE  24  a 
Mortality  of  London  boroughs  grouped  by  wealth.     (Frutn  Stevenson) 


Domestic  servants 
(both  sexes)  per  cent, 
of  population  (1911) 

Deatl 

i-rate 

Infant  mortality 

Death-rat« 

from 

1911-13 

1918-19 

1911-1. 

tuh»T(  uloBJi, 

1911-13 

(V 

O 

1 

T3 

oS-rt 

T3  O 

C  « 

«■" 

(XI 

B 

1 

o 

V 

3 

u 

1 

Kensinizton 

16.67 
16.40 
15.17 
14.96 
12.98 
10.42 

13.7 
10.4 
12.6 
14.7 
14.3 
13.3 

13.6 
11.0 
13.3 
14.0 
14.6 
13.2 

83 
64 

77 
78 
79 
88 

221 

236 
235 
155 
250 
237 

112 

72 
94 
91 
98 
109 

1.32 

0.81 
1.49 
1 .  64 
1.70 
1.33 

1.32 

HamDstead 

0.80 

Westminster 

Chelsea 

1 .  42 
1  r,l 

Marvlebone 

1.66 

Paddineton 

1.31 

Group  I 

14.38 

13.2 

13.4 

80 

228 

100 

1.39 

1.36 

City 

6.46 
5.71 
5.67 
4.98 
4.38 
4.10 

14.0 
11.3 
11.5 
13.0 
15.1 
13.9 

14.6 
11.1 
11.6 
12.4 
15.2 
13.7 

122 
51 

72 
71 
99 
93 

278 
294 
240 
231 
267 
349 

97 
84 
96 
85 
102 
102 

1 .  95 
1.09 
1.20 
1.30 
2.30 
1.60 

1.84 

^^"■^j  _ 

Lewisham 

1.01 

Wandsworth 

Stoke  Newington  .... 
Holborn 

1.18 
1.28 
2.17 

Greenwich 

1.59 

Group  II 

5.34 

12.2 

12.1 

73 

272 

94 

1.32 

1.30 

Fulham 

3.52 
3.30 
3.18 
3.12 
2.95 
2.81 
2.68 
2.64 
2.62 
2.48 

13.6 
14.5 
14.3 
15.1 
13.5 
12.6 
13.8 
15.0 
13.6 
14.9 

14.1 
14.3 
14.0 
15.1 
13.6 
12.9 
13.6 
14.8 
13.7 
14.5 

85 
91 

82 
81 
83 
88 
83 
87 
74 
88 

222 
207 
217 
226 
355 
220 
268 
176 
276 
258 

105 

114 

105 

98 

100 

84 

99 

117 

107 

107 

1.73 
1.62 
1.71 
1.91 
1.68 
1.67 
1.61 
1.73 
1.56 
1 .  69 

1.69 

Hammersmith 

Lambeth 

1.58 
1.68 

St.  Pancras 

1.85 

Hacknev 

1.67 

Woolwich 

1.65 

Camberwell 

1.60 

Deotford 

1.70 

Battersea 

1.53 

Ishngton 

1.66 

Group  III 

2.90 

14.1 

14.0 

84 

243 

103 

1.70 

1.67 

Stepnev 

1.33 
1.24 
1.23 
1.18 
0.97 
0.91 
0.77 

15.8 
18.6 
17.5 
17.2 
17.8 
18.9 
16.4 

16.5 
18.4 
17.6 
17.0 
17.8 
19.5 
17.1 

90 
91 
101 
92 
105 
124 
101 

314 
229 

225 
216 
360 
255 
263 

121 

137 
V2'2 
125 
133 
150 
123 

2.15 
2.47 
2  23 
1.88 
2.35 
2.47 
2.21 

2  12 

Finsbury 

2.45 

Southwark 

2.17 

Poplar 

1.86 

Bermondsev 

2.31 

Shoreditch 

2.46 

Bethnal  Green 

2.21 

Group  IV 

1.13 

17.1 

17.4 

99 

260 

128 

2.21 

2.18 

County  of  London  .  . . 

4.74 

14.4 

14.4 

86 

247 

109 

1.71 

1.68 

208  BIOLOGY  OF  DEATH 

richest  group.  Indeed,  the  difference  between  the  first  three  London 
groups  is  slight,  significant  excess  only  being  apparent  for  the  poorest 
group.  And  whereas  the  excess  of  mortality  of  the  poorest  over  the 
richest  group  in  Paris  is  104  per  cent.,  in  London  it  is  only  30  per  cent." 

He  then  examines  the  question  as  to  whether  the  dis- 
crepancies may  be  due  to  differences  in  the  method  of  con- 
struction of  the  two  sets  of  mortality  figures  and  concludes : 

**That  the  remarkable  contrast  in  experience  between  the  two  cities 
cannot  be  explained,  except  possibly  in  a  very  minor  degree,  by  any 
differences  of  method  in  compilation  of  the  statistics  compared." 

Stevenson  then  goes  on  to,  the  discussion  of  infant 
mortality  and  says : 

"The  conclusion  just  arrived  at  applies  still  more  to  infant  than  to 
total  mortality,  for,  in  its  case,  the  contrast  between  rich  and  poor  quarters 
of  Paris  assumes  dimensions  which,  in  the  light  of  London  experience,  seem 
quite  fantastic." 

Eegarding  mortality  from  tuberculosis  the  London 
experience  again  fails  to  agree  with  the  Paris  experience, 
and  Hersch's  conclusions  from  the  data  of  the  latter  city 
would  be  absurd  if  applied  to  the  former. 

EXPERIMENTS  ON  TEMPERATURE  AND  DURATION   OF  LIFE 

Altogether  it  is  plain  that  we  need  another  kind  of 
evidence  than  the  simple  unanalyzed  parallelism  which 
Hersch  demonstrates  between  poverty  and  the  general 
death  rate  if  we  are  to  get  any  deep  understanding  of  the 
influence  of  environmental  circumstances  upon  the  dura- 
tion of  life  or  the  general  death  rate.  We  shall  do  well 
to  turn  again  to  the  experimental  method.  About  a 
dozen  years  ago  Loeb, 

starting  from  the  idea  that  chemical  conditions  in  the  organism  are  one 
of  the  main  variables  in  this  case,  raised  the  question  whether  there  was  a 
definite  coefficient  for  the  duration  of  life  and  whether  this  temperature 
coefficient  was  of  the  order  of  magnitude  of  that  of  a  chemical  reaction. 
The  first  experiments  were  made  on  the  unfertilized  and  fertilized  eggs 


STUDIES  ON  THE  DURATION  OF  LIFE     209 

of  the  sea  urchin  and  could  only  be  carried  out  at  the  upper  temperature 
limits  of  the  organism,  since  at  ordinary  temperatures  this  organiHm  live* 
for  years.  In  the  upper  temperature  region  the  temperature  coeflicient 
for  the  duration  of  life  was  very  high,  probably  on  account  of  the  fact 
that,  at  this  upper  zone  of  temperature,  death  is  determined  by  a  change 
of  the  nature  of  a  coagulation  or  some  other  destructive  procoHH.  Moore, 
at  the  suggestion  of  Loeb,  investigated  the  temperature  coefficient  for  the 
duration  of  life  for  the  hydranth  of  a  tubularian  at  the  upper  temperature 
limit  and  found  that  it  was  of  the  same  order  of  magnitude  as  that 
previously  found  for  the  sea  urchin  egg.  In  order  to  prove  that  there 
is  a  temperature  coefficient  for  the  duration  of  life  throughout  the  whole 
scale  of  temperatures  at  which  an  organism  can  live,  experiments  were 
required  on  a  form  whose  duration  of  life  was  short  enough  to  measure 
the  duration  of  life  even  at  the  lowest  temperature. 

A  suitable  organism  was  found  in  Drosophila.  This 
was  groA\Ti  under  aseptic  conditions,  as  already  described. 
The  general  results  are  shown  in  Table  25. 

TABLE  25 

Effect  of  teinperature  on  duration  of  life  of  Drosophila. 
{After  Loeb  and  Northrop) 


Duration  (in  daya)  of 

Temperature 

Larval  stage 

Pupal  stage 

Life  of 
imago 

Total  duration 

oi  liie  from  tgg 

tu  death 

°c 

10 
15 

57 
17.8 

Pupae  die 
iLl3.7ljf 

:     120.5 
it92.4^ 

177.5  ^-x 
123.9 

20 

7.77 

6.33 

40.2 

54.3 

25 

5.82 

4.23 

28.5 

38.5 

27.5 

(4.15) 

3.20 

.... 

•  •   •  • 

30 

4.12 

3.43 

13.  G 

21.15 

From  this  table  it  is  seen  that  at  the  lowest  tempera- 
ture the  duration  of  life  is  longest,  and  at  the  highest  tem- 
perature shortest.  Cold  slows  up  the  rate  of  living  for 
the  fly.  Heat  hastens  it.  One  gathers,  from  the  account 
which  Loeb  and  Northrop  give  of  the  work,  that  at  low 
temperature  the  flies   are  sluggish  and  inactive  in  all 

14 


210  BIOLOGY  OF  DEATH 

three  developmental  stages  and  perhaps  live  a  long  time 
because  they  live  slowly.  At  high  temperatures,  on  the 
other  hand,  the  fly  is  very  active  and  lives  its  life  through 
quickly  at  the  pace  that  kiUs/'  These  results  are  exactly 
comparable  to  the  effect  of  a  regular  increase  of  tempera- 
ture upon  a  chemical  reaction.  Indeed,  Loeb  and  North- 
rop consider  that  their  results  prove  that 

With  a  supply  of  proper  and  adequate  food  the  duration  of  the  larval 
stage  is  an  unequivocal  function  of  the  temperature  at  which  the  larvae  are 
raised,  and  the  temperature  coefficient  is  of  the  order  of  magnitude  of  that 
of  a  chemical  reaction,  i.  e.,  about  2  or  more  for  a  difference  of  10°  C.  It 
increases  at  the  lower  and  is  less  at  the  higher  temperatures.  The  duration 
of  the  pupal  stage  of  the  fly  is  also  an  unequivocal  function  of  the  tempera- 
ture and  the  temperature  coefficient  is  for  each  temperature  practically 
identical  with  that  for  the  larval  stage.  The  duration  of  life  of  the  imaiio 
is,  with  proper  food,  also  an  unequivocal  function  of  the  temperature  and 
the  temperature  coefficient  for  the  duration  of  life  is,  within  the  normal 
temperature  limits,  approximately  identical  with  that  for  the  duration  of 
life  of  the  larva  and  pupa. 

How  are  these  results  to  be  reconciled  with  the  pre- 
vious finding  that  heredity  is  a  primary  factor  in  the 
determination  of  duration  of  life  of  Drosophilaf  We 
have  here,  on  first  impression  at  least,  an  excellent  exam- 
ple of  what  one  always  encounters  in  critical  genetic 
investigations:  the  complementary  relations  of  heredity 
and  environment.  In  our  experiments  a  general  mixed 
population  of  Drosophila  kept  under  constant  environ- 
ment was  shown  to  be  separable  by  selection  into  a  num- 
ber of  very  diverse  strains  in  respect  of  duration  of  life. 
In  Loeb  and  Northrop 's  experiments,  a  general  mixed 
population  of  Drosophila,  but  of  presumably  constant 
genetic  constitution,  at  least  approximately  such,  through- 
out the  experiment,  was  sllo^vn  to  exhibit  changes  of 
duration  of  life  with  changing  environments.  It  is  the 
old  familiar  deadlock.     Heredity  constant  plus  changing 


STUDIES  ON  THE  DURATION  OF  LIFE     211 

environment  equals  diversity.  EnvirnnrrKMil  mnst.-nit 
phis  varying  hereditary  constitution  also  equals  diversity. 
Can  we  penetrate  no  farther  than  this  into  the  matter? 
I  think  in  the  present  case  we  can.  In  Loch  and  Northrop 's 
experiments,  temperature  and  duration  of  life  were  not 
the  only  two  things  that  varied.  The  difff^roTit  tempera- 
ture groups  also  differed  from  each  other — because  of  the 
temperature  differences,  to  he  sure,  hut  not  less  really — 
in  respect  of  general  metaholic  aci'iviiij,  expressed  in 
muscular  movement  and  every  other  way.  In  the  gene- 
tic experiments  metabolic  activity  was  suhstantially  equal 
in  all  the  hereditarily  different  lines.  The  idea  suggests 
itself,  both  on  a  priori  grounds  and  also  upon  the  basis 
of  certain  experimental  data  presently  to  be  in  part  re- 
viewed, that  possibly  duration  of  life  may  be  an  implicit 
function  of  only  the  two  variables 

a.  Genetic  constitution 

b.  Rate  of  metabolic  activity. 

The  functional  relations  of  metabolic  activity  with 
temperature,  food,  light  and  other  environmental  fac- 
tors are  all  well  known.  For  present  purposes  we  do 
not  need  to  go  into  the  question  of  their  exact  form.  The 
essential  point  is  that  all  these  en^'iroimiental  factors 
stand  in  definite  functional  relations  to  rate  of  metabolic 
activity,  and  do  not  so  stand  in  relation  to  genetic  consti- 
tution. Genetic  constitution  is  not  a  function  of  the 
environment,  but  is,  for  any  individual,  a  constant,  and 
only  varies  between  individuals. 

This  mav  be  thouc:ht  merelv  to  be  an  involved  wav  of 
saying  what  one  knows  a  priori:  namely,  that  duration 
of  life,  in  general  and  in  particular,  depends  only  upon 
heredity  and  environment.  So  in  one  sense  it  is.  But 
the  essential  point  I  would  make  here  is  that  the  wanner 


212  BIOLOGY  OF  DEATH 

in  which  the  environmental  forces  (of  suh-lethal  inten- 
sity, of  course)  chiefly  act  in  determining  duration  of 
life,  appears  to  he  hy  changing  the  rate  of  metabolism  of 
the  individual.  Furthermore  one  would  suggest,  on  this 
view,  that  what  heredity  does  in  relation  to  duration  of 
life  is  chiefly  to  determine,  within  fairly  narrow  limits, 
the  total  energy  output  which  the  individual  can  exhibit 
in  its  life  time.  This  limitation  is  directly  brought  about 
presumably  through  two  general  factors:  viz,  (a)  the 
kind  or  quality  of  material  of  which  this  particular  vital 
machine  is  built,  and  (b)  the  manner  in  which  the  parts 
are  put  together  or  assembled.  Both  of  these  factors 
are,  of  course,  expressions  of  the  extent  and  character 
of  the  processes  of  organic  evolution  which  have  given 
rise  to  this  particular  species  about  which  we  may  be 
talking  in  a  particular  instance. 

There  is  some  direct  experimental  evidence,  small  in 
amount  to  be  sure,  but  exact  and  pertinent,  to  the  effect 
that  the  duration  of  life  of  an  animal  stands  in  inverse  re- 
lation to  the  total  amount  of  its  metabolic  activity,  or  put 
in  other  words,  to  the  work,  in  the  sense  of  theoretical 
mechanics,  that  it  as  a  machine  does  during  its  life. 
Slonaker  kept  4  albino  rats  in  cages  like  the  old  fashioned 
revolving  squirrel  cages,  with  a  properly  calibrated  odo- 
meter attached  to  the  axle,  so  that  the  total  amount  of 
running  which  they  did  in  their  whole  lives  could  be 
recorded.     The  results  were  those  shown  in  Table  26. 

It  will  be  perceived  that  the  amount  of  exercise  taken 
by  these  rats  was  astonishingly  large.  For  a  rat  to 
run  5,447  miles  in  the  course  of  its  life  is  indeed  a  re- 
markable performance.  Now  these  4  rats  attained  an 
average  age  at  death  of  29.5  months.  But  three  control 
rats  confined  in  stationary  cages  so  that  they  could  only 


STUDIES  ON  THE  DURATION  OF  LIFE     213 

move  about  to  a  limited  degree,  but  otherwise  under 
conditions,  including  temperature,  identical  with  those 
in  the  revolving  cages,  attained  an  average  age  at  death 
of  40.3  months.     All  were  stated  to  have  died  of  **old 

TABLE  26 
Relation  of  longevity  to  muscular  activity  in  rats     (Slonaker) 

TOTAL  NUMBER  OF  MILES  RUN  DURING  LIFE 


Age  in  months 
at  death 

Rat  No.  1 
Miles 

No.  4 

Miles 

No.  2 
Miles 

No.  3 

Ml  lea 

25 

1265 

1391 

2098 

26 

32 

34 

5447 

7  > 


age. ' '  From  this  experiment  it  clearly  appears  that  the 
greater  the  total  work  done,  or  total  energy  output,  the 
shorter  the  duration  of  life,  and  vice  versa.  Or,  put 
another  way,  if  the  total  activity  per  unit  of  time  is  in- 
creased by  some  means  other  than  increasing  tempera- 
ture, the  same  results  appear  as  if  the  increased  activity 
is  caused  by  increased  temperature.  It  appears,  in 
short,  to  be  acti\'ity  per  se,  and  not  the  temperature  prr 
se  that  is  of  real  significance.  There  is  other  evidence, 
for  which  space  lacks  here,  pointing  in  the  same  direction. 
An  entirely  different,  and  extremely  suggestive  line 
of  evidence  in  favor  of  the  view  here  set  forth,  has  been 
given  by  Professor  Max  Eubner,  the  distinguished  Ger- 
man student  of  the  energy  relations  of  the  living  organ- 
ism. Studying  a  considerable  range  of  animals,  he  has 
found  that  all  transform  nearly  the  same  total  amount 
of  energy,  per  kilo  of  body  iveight,  in  the  whole  period 
from  their  birth  to  their  natural  death.  The  mean  value 
of  the  constant  Kubner  finds  to  be  191,600  calories,  the 
values  for  different  species  ranging  betwx^en  141,090  and 


214  BIOLOGY^ OF  DEATH 

265,500  calories.  Small  animals,  with  an  intensive  meta- 
bolism live  a  relatively  short  time;  large  animals  with 
more  sluggish  metabolism  live  a  longer  time.  Eubner's 
view  is  that  a  definite  sum  of  living  action  (energy  trans- 
formation) determines  the  physiological  end  of  life. 
This  is  precisely  the  view  suggested  here  except  that  it 
is  here  postulated  that  the  definite  sum,  for  individual 
or  species,  is  fundamentally  determined  by  heredity, 
working  through  the  structural  make-up. 

If  we  may  be  permitted  to  make  a  suggestion  regard- 
ing the  interpretation  of  Loeb  and  Northrop 's  results  in 
conjunction  with  our  own  on  Drosophila,  it  would  be  to 
this  effect.  Any  given  genetically  pure  strain  of  Droso- 
pJiila  is  made  up  of  individual  machines,  constructed  to 
turn  out,  before  breaking  down,  a  definite  limited  amount 
of  energy  in  the  form  of  work,  mechanical,  chemical  and 
other.  This  definitely  limited  total  energy  output  is 
predetermined  by  the  hereditary  constitution  of  the  indi- 
vidual which  fixes  the  kind  of  physico-chemical  machine 
that  that  individual  is.  But  the  rate  per  unit  of  time  of 
the  energy  output  may  be  influenced  between  wide  limits 
by  environmental  circumstances  in  general  and  tempera- 
ture in  particular,  since  increased  temperature  increases 
rate  of  metabolic  chemical  changes  in  about  the  same 
ratio,  as  demonstrated  by  a  wealth  of  work  on  tempera- 
ture coefficients,  as  it  increases  other  chemical  changes. 
But  if  the  rate  of  energy  outputper  unit  of  time  is  changed, 
the  total  time  taken  for  the  total  output  of  a  predeter- 
mined amount  of  energy,  as  work,  must  change  in  inverse 
proportion  to  the  change  of  rate.  So  we  should  expect 
just  precisely  the  results  on  duration  of  life  that  Loeb 
and  Northrop  got,  and  so  far  from  these  results  being  in 
contradiction  to  ours  upon  heredity,  they  may  be  looked 


STUDIES  ON  THE  DURATION  OF  LIFE     215 

upon  as  a  necessary  consequence  of  them.  Luel>  and 
Northrop 's  iinal  conchision  is:  *'The  obsers^ations  on  the 
temperature  coefficient  for  the  duration  of  life  su^^^est 
that  this  duration  is  determined  by  the  ])r()dnction  of  a 
substance  leading  to  old  age  and  natural  death,  or  by  the 
destruction  of  a  substance  or  substances,  whicli  normally 
prevent  old  age  and  natural  death."  Tlir  view  wliich  I 
have  here  suggested,  completely  incorporates  this  view 
within  itself,  if  we  suppose  that  the  total  amount  of  hypo- 
thetical ^^  substance  or  substances  which  normally  prevent 
old  age  and  natural  death"  was  essentially  determined 
by  heredity. 

This  view  I  take  to  be  in  no  wav  necessarilv  or  funda- 
mentally  contradictory  to  that  set  forth  in  this  work. 
Whatever  the  factor  whicli  determines  specific  longev- 
ity may  be;  whether  a  specific  chemical  substance,  as 
Loeb  and  Northrop  suggest,  or  more  generally,  as  T  have 
suggested,  the  kind  of  material,  in  the  sense  of  its  biologi- 
cal fitness,  composing  the  multicellular  body,  and  the 
nature  of  the  organization  (in  detail)  of  that  material 
to  form  the  multicellular  bodv;  it  seems  to  me  that  we 
have  now  a  sufficient  mass  of  critical  evidence  to  say 
that  it  is  proved  that  quantitatively  the  effective  magni- 
tude of  tliis  specific  longevity  factor  in  each  particular 
case  is  determined  hy  heredity.  This  I  take  to  be  of 
greater  importance  than  the  precise  nature  of  the  specific 
longevity  factor  itself,  about  which  we  are,  admittedly, 
entirely  ignorant.  I  can  see  nothing  in  the  availal)le  evi- 
dence wliich  definitely  makes  Loeb's  suggestion  inherently 
more  probable  than  mine.  It  does,  however,  seem  clear 
that,  by  definitely  showing  the  significance  of  tlie  lieredity 
element  in  the  problem,  helj)  has  been  rendered  the  prog- 
ress of  future  research  in  the  field. 


216  BIOLOGY  OF  DEATH 

It  would  seem,  at  first  thought,  that  one  should  be 
able  to  test  the  theory  here  suggested,  that  rate  of  energy 
expenditure  in  the  business  of  living  is  negatively  corre- 
lated mth  the  total  duration  of  life,  by  an  examination  of 
the  mortality  rates  for  persons  in  different  occupations 
as  set  forth,  for  example,  in  the  well  known  paper  of 
Bertillon.  "When  one  endeavors  to  make  such  a  test, 
however,  he  is  at  once  confronted  with  a  series  of  diffi- 
culties which  presently  convince  him  that  the  project 
is  virtually  an  impossible  one,  if  he  wishes  critical  results. 
In  the  first  place,  mean  age  at  death  will  not  do  as  a 
criterion,  because  of  the  great  differences  in  the"  age  dis- 
tributions of  those  engaged  in  different  occupations. 
This  point  has  lately  been  thoroughly  discussed  by  Collis 
and  Greenwood,  in  their  book  ' '  The  Health  of  the  Indus- 
trial Worker. ' '  Indeed,  their  whole  treatment  of  the  prob- 
lem of  occupational  mortality  is  by  far  the  most  sound 
and  critical  which  the  present  writer  has  yet  seen.  One 
must  deal  with  age  and  sex  specific  death  rates,  or  mor- 
tality indices  based  upon  them. 

In  the  second  place,  there  are  specific  hazards,  direct 
or  indirect,  in  various  occupations,  quite  apart  from  any 
question  of  energy  expenditure  involved  in  the  case. 
These  hazards  will,  obviously,  tend  to  obscure  any  direct 
eifects  of  the  energy  relations  involved. 

In  the  third  place,  we  have  only  the  merest  suggestion 
of  quantitatively  accurate  loiowledge  as  to  the  average 
energy  output  involved  indifferent  trades  and  occupations. 

On  the  last  point,  a  beginning  to  collect  information 
has  been  made  by  Waller  and  his  co-workers.  In  a  re- 
cent paper  Waller  and  De  Decker  have  given  the  mean 
calory  output,  per  hour,  per  square  meter  of  body  surface 
for  a  small  sample  of  workers  in  a  few  trades.     But  the  re- 


STUDIES  ON  THE  DURATION  OF  TJFE      217 

suits  are  far  too  meager,  and,  statistically,  too  unrepre- 
sentative to  warrant  any  attempt  at  generalization  from 
the  present  point  of  view. 

As  in  so  many  other  cases  the  experimental  method  is 
likely  to  shed  far  more  critical  light  on  this  problem  than 
is  the  purely  statistical  method  dealing  with  human  data. 
There  are  too  many  factors  in  the  latter  material  that 
cannot  be  controlled. 

GONADS  AND  DURATION  OF  LIFE 

There  is  another  and  quite  different  line  of  experi- 
mental work  on  the  duration  of  life  which  mav  be  touched 
upon  briefly.  The  daily  press  has  lately  had  a  great  deal 
to  say  about  rejuvenation,  accomplished  by  means  of 
various  surgical  procedures  undertaken  upon  the  primary 
sex  organs,  particularly  in  the  male.  Tliis  newspaper 
notoriety  has  especially  centered  about  the  work  of 
Voronotf  and  Steinach.  The  only  experiments  wliich,  at 
the  present  time,  probably  deserve  serious  consideration 
are  those  of  Steinach.  He  has  worked  chiefly  with  white 
rats.  His  theory  is  that,  by  causing  through  approjiriate 
operative  procedure,  an  extensive  regeneration,  in  a  sen- 
ile animal  about  to  die,  of  certain  glandular  elements  of 
the  testis,  senility  and  natural  death  will  for  n  timo  be 
postponed  because  of  the  internal  secretion  i)()ure(l  into 
the  blood  by  the  regenerated  ''puberty  glands"  as  he  calls 
them.  The  operation  wliich  he  finds  to  be  most  effective 
is  to  ligate  firmly  the  efferent  duct  of  the  testis,  through 
which  the  sperm  normally  pass,  close  u]>  to  the  testis 
itself,  and  before  the  coiled  portion  of  the  duct  is  reached. 
The  result  of  tliis,  according  to  Steinacirs  account,  is  to 
bring  about  in  highly  senile  animals  a  groat  enlargement 
of  all  the  sex  organs,  a  return  of  sexual  activity, previously 


218  BIOLOGY  OF  DEATH 

lost  through  old  age,  and  a  general  loss  of  senile  bodily 
characteristics  and  a  resumption  of  the  conditions  of 
full  adult  vigor  in  those  respects,  together  with  a  consid- 
erable increase  in  the  total  duration  of  life. 

Space  is  lacking  to  go  into  the  many  details  of 
Steinach's  work,  much  of  which  is  indeed  chiefly  of  inter- 
est only  to  the  technical  biologist,  and  from  a  wholly 
different  standpoint  than  the  present  one.  I  should, 
however,  like  to  present  one  example  from  his  experi- 
ments. As  control,  a  rat  was  taken,  in  the  last  degree 
senile.  He  was  26  months  old  when  the  experiment  be- 
gan. He  was  obviously  emaciated,  had  lost  much  of  his 
hair,  particularly  on  the  back  and  hind  quarters.  He 
was  weak,  inactive  and  drowsy,  as  indicated  by  the  fact 
that  his  eyes  were  closed,  and  were,  one  infers  from 
Steinach,  kept  so  much  of  the  time. 

A  litter  brother  of  this  animal  had  the  efferent  ducts 
of  the  testes  ligated.  This  animal,  we  are  told,  was,  at 
the  time  of  the  operation,  in  so  much  worse  condition  of 
senility  than  his  brother,  above  described,  that  it  was  not 
thought  worth  while  even  to  photograph  him.  His  con- 
dition was  considered  hopeless.  To  the  surprise  of  the 
operator,  however,  he  came  back,  slowly  but  surely  after 
the  operation,  and  after  three  and  a  half  months  pre- 
sented a  perfect  picture  of  lusty  young  rathood.  He 
was  in  full  vigor  of  every  sort,  including  sexual.  He 
outlived  his  brother  by  8  months,  and  himself  lived  10 
months  after  the  operation,  at  which  time  he  was,  accord- 
ing to  Steinach,  practically  moribund.  This  represents  a 
presumptive  lengthening  of  his  expected  span  of  life  by 
roughly  a  quarter  to  a  third.  It  is  to  he  rememhered, 
however,  that  Slonaker's  rats  to  which  nothing  was  done 
lived  to  an  average  age  of  40  moyiths. 


STUDIES  ON  THE  DURATION  OF  LIFE     219 

The  presumption  that  Stoinacli^s  experinuMits  have 
really  brought  al)oiit  a  statistically  sigiiiiicant  h-ngthen- 
ing  of  life  is  large,  and  the  basis  of  ascertained  fact 
small.  After  a  careful  examination  of  Steinach\s  ])ril- 
liant  contribution,  one  is  compelled  to  take  the  view  that, 
however  interesting  the  results  may  be  from  the  stand- 
point of  functional  rejuvenation  in  the  sexual  sphere, 
the  case  is  not  proven  that  any  really  signilicant  length- 
ening of  the  life  span  has  occurred.  In  ojdor  to  prove 
such  a  lengthening  we  must,  first  of  all,  have  abundant  and 
accurate  quantitative  data  as  to  the  normal  variation  of 
normal  rats  in  respect  of  duration  of  life,  and  then  show, 
having  regard  to  the  probable  errors  involved,  that  the 
mean  duration  of  life  after  the  operation  has  been  signi- 
ficantly lengthened.  This  Steinach  does  not  do.  His 
paper  is  singularly  bare  of  statistical  data.  We  may  well 
await  adequate  quantitative  evidence  before  attempting 
any  general  interpretation  of  his  results. 

Indeed,  one  may  note  in  passing  that  the  case  does 
not  seem  entirely  clear  in  respect  of  Steinach  *s  results 
in  the  purely  sexual  sphere.  Thus  Romeis  has  repeated 
the  experiments,  and  finds,  from  comparative  liistologi- 
cal  studies  on  the  genital  organs  of  rats,  before  and  aft>er 
Steinach 's  operation,  that  there  is  no  evidence  of  any 
increase  in  Leydig's  interstitial  cells,  and  hence  none 
of  the  so-called  ^interstitial  or  puberty  gland."  Komeis 
noted  no  increase  in  sexual  desire  among  his  rats  after 
the  operation.  The  hypertrophy  of  the  seminal  vesicles 
and  prostate,  described  by  Steinach  following  the  opera- 
tion, was  also  seen  by  Romeis,  but  found,  by  the  latter,  to 
be  merely  the  result  of  the  stasis  of  tlie  secretions  nec- 
essarily consequent  upon  the  operation,  and  not  a  true 
functional  hypertrophy  at  all. 


220 


BIOLOGY  OF  DEATH 


THE  PITUITARY  GLAND  AND  DURATION  OF  LIFE 

Eobertson  has  been  engaged  for  a  number  of  years 
past  on  an  extensive  series  of  experiments  regarding  the 
effect  of  various  agents  upon  the  growth  of  white  mice. 
The  experiments  have  been  conducted  with  great  care 
and  attention  to  the  proper  husbandry  of  the  animals. 
In  consequence,  the  results  have  a  high  degree  of  trust- 
worthiness. In  the  course  of  these  studies  he  found  that 
the  anterior  lobe  of  the  pituitary  body,  a  small  gland  at 
the  base  of  the  brain,  normally  secretes  into  the  blood- 
stream minute  amounts  of  an  active  substance  which  has 
a  marked  effect  upon  the  normal  rate  of  growth.  By  chemi- 
cal means,  Robertson  was  able  to  extract  this  active  sub- 
stance from  the  gland  in  a  fairly  pure  state,  and  gave  to  it 
the  name  tethelin.  In  later  experiments,  the  effect  of 
tethelin,  given  by  the  mouth  mth  the  food,  was  tried  in 
a  variety  of  ways. 

In  a  recent  paper,  Eobertson  and  Eay  have  studied 
the  effect  of  this  material  upon  the  duration  of  life  of  the 
white  mouse  with  the  results  shown  in  Table  27. 

TABLE  27 
Effect  of  tethelin  on  duration  of  life  in  days  of  white  mice. 

(Robertson  and  Ray) 


MALES 

FEMALES 

Both 

sexes 

together 

Class  of 
animals 

Average 

duration 

of  life 

Dev. 

from 
normal 

Dev. 
P.  E. 

Chance 
dev.  was 
acciden- 
tal 

Average 

duration 

of  life 

a  Dev. 
'from 
normal 

Dev. 
P.  E. 

Chance 
dev.  was 
acciden- 
tal 

Chance 
dev.  was 
acci- 
dental 

Normal 
Tethelin 

767 
866 

719 
800 

+99 

3.00 

1:22.25 

+81 

2.25 

1:6.75 

1:150.2 

From  this  table,  it  is  apparent  that  the  administration 
of  tethelin  with  the  food  from  birth  to  death  prolonged 


STUDIES  ON  THE  DURATION  OF  LIFE     221 

life  to  a  degree  which,  in  the  case  of  the  males,  mav  be 
regarded  as  probablj^  significant  statistically.  In  the 
case  of  the  females,  where  the  ratio  of  the  deviation  to 
its  probable  error  (Dev. /P.  E.)  falls  to  2.25  the  case 
is  very  doubtful.  The  procedure  by  which  the  chance  of 
1 :150.2  that  results  in  both  sexes  together  were  acciden- 
tal, was  obtained  is  of  doubtful  validity.  Putting  males 
and  females  together  from  the  original  table,  I  find  the 
following  results. 

TABLE  28 

Duration  of  life  of  white  mice,  both  sexes  taken  together 

{From  data  of  Robertson  and  Ray) 


Age 
Group 

No. of 

deaths 

of  normals 

(Both  sexes) 

No.  of  deaths 

of  tethelin 

fed 

(Both  sexes) 

200-299 

3 

Tethelin  fed:  Mean  age  at  death  =839 ±20 

300-399 

2 

,  . 

Normal   fed:  Mean  age  at  death  ^=743±17 

400-499 

2 

1 

Difference                      96±26 

500-599 
600-699 

9 

7 

3 
9 

Difference  =  3.7 
P-  ^-  Diff. 

700-799 

15 

.   . 

800-899 

10 

10 

900-999 

10 

6 

1000-1099 

6 

9 

1100-1199 

1 

64 

39 

One  concludes  from  these  figures  that  tethelin  can  be 
regarded  as  having  lengthened  the  span  of  life  to  a  de- 
gree wliich  is  just  significant  statistically.  One  would 
expect,  from  the  variation  of  random  sampling  alone,  to 
get  as  divergent  results  as  these  about  IV'i  times  in  every 
100  trials  mth  samples  of  64  and  39,  respectively. 

In  any  event  it  is  apparent  that,  making  out  the  best 
case  possible,  the  differences  in  average  duration  of  life 


222  BIOLOGY  OF  DEATH 

produced  by  administration  of  tethelin  are  of  a  wholly 
different  and  smaller  order  than  those  which  have  been 
shown,  in  the  earlier  portion  of  this  chapter,  to  exist  be- 
tween pure  strains  of  Brosopliila  which  are  based  upon 
hereditary  differences. 

Putting  together  all  the  results  which  have  been  re- 
viewed in  this  and  the  preceding  chapter,  it  appears  to 
be  clearly  and  firmly  established  that  inheritance  is  the 
factor  of  prime  importance  in  determining  the  normal, 
natural  duration  of  life.  In  comparison  Avith  this  factor, 
the  influence  of  environmental  forces  (of  sub-lethal  im- 
mediate intensity  of  course)  appears  in  general  to  be 
less  marked. 


CHAPTER  VIII 

NATURAL  DEATH,  PUBLIC  HEALTH,  AXD  TIIK 

POPULATION  PROBLEM. 

SUMMARY  OF  RESULTS 

I  have  attempted  to  review  some  of  the  imi)()rtant 
biological  and  statistical  contributions  wliich  have  been 
made  to  the  knowledge  of  natural  death  and  the  duration 
of  life,  and  to  synthesize  these  scattered  results  into 
a  coherent  unified  whole.  In  the  present  chapter  I  shall 
endeavor  to  summarize,  in  the  briefest  way,  the  scattered 
facts  which  have  been  passed  in  review,  and  to  follow  a 
presentation  of  the  general  results  to  which  they  lead 
with  some  discussion  of  what  we  may  reasonably  regard 
the  future  as  having  in  store  for  us,  so  far  as  may  be 
judged  from  our  present  knowledge  of  the  trend  of  events. 

What  are  the  general  results  of  our  review  of  the  gen- 
eral biology  of  death?  In  the  first  place,  one  perceives  that 
natural  death  is  a  relatively  new  thing,  which  appeared 
first  in  evolution  when  differentiation  of  cells  for  ]^artic- 
ular  functions  came  into  existence.  Unicellular  ani- 
mals are,  and  always  have  been,  immortal.  The  cells  of 
higher  organisms,  set  apart  for  reproduction  in  the 
course  of  differentiation  during  evolution,  are  Immortal. 
The  only  requisite  conditions  to  make  their  potential  im- 
mortality actual  are  physico-chemical  in  nature  and  are 
now  fairly  well  understood,  particularly  as  a  result  t)f 
the  investigations  of  Loeb  upon  artificial  ])arthenogenesis 
and  related  phenomena.     The  essential   and  important 

2'J3 


224  BIOLOGY  OF  DEATH 

somatic  cells  of  the  body,  however  much  differentiated, 
are  also  potentially  immortal;  but  the  conditions  neces- 
sary for  the  actual  realization  of  the  potential  immor- 
tality are,  in  the  nature  of  the  case,  as  has  been  shown 
by  the  brilliant  researches  of  Leo  Loeb,  Harrison  and 
Carrel  on  tissue  culture,  such  as  cannot  be  realized  so 
long  as  these  cells  are  actually  in  and  a  part  of  the  higher 
metazoan  body.  The  reason  why  this  is  so,  and  why  in 
consequence  death  results  in  the  metazoa,  is  that,  in  such 
organisms  the  specialization  of  structure  and  function 
necessarily  makes  the  several  parts  of  the  body  mutually 
dependent  for  their  life  upon  each  other.  If  one  organ 
or  group,  for  any  accidental  reason  begins  to  function 
abnormally  and  finally  breaks  down,  the  balance  of  the 
whole  is  upset  and  death  eventually  follows.  But  the 
individual  cells,  themselves,  could  go  on  living  indefinitely, 
if  they  were  freed,  as  they  are  in  cultures,  of  the  neces^ 
sity  of  depending  upon  the  proper  functioning  of  other 
cells  for  their  food,  oxygen,  etc. 

So  then  we  see  emerging,  as  our  first  general  result, 
the  fact  that  natural  death  is  not  a  necessary  or  inevit- 
able consequence  of  life.  It  is  not  an  attribute  of  the 
cell.  It  is  a  by-product  of  progressive  evolution — the 
price  we  pay  for  differentiation  and  specialization  of 
structure  and  function. 

This  first  result  indicates  logically,  in  any  particu- 
lar organism  such  as  man,  the  great  importance  of 
a  quantitative  analysis  of  the  manner  in  which  dif- 
ferent parts  of  the  body  break  down  and  lead  to  death. 
Such  an  analysis,  carefully  worked  through,  demonstrates 
that  this  breaking  down  is  not  a  haphazard  process,  but 
a  highly  orderly  one  resting  upon  a  fundamental  biolog- 
ical basis.     The  progress  of  the  basic  tissue  elements 


NATURAL  DEATH,  PUBLIC  HEALTH    22; 


of  the  body  along  the  evolutionary  pathway  appears  to  be 
an  important  factor  in  determining  tlie  time  wlien  the 
organ  systems  in  which  they  are  chiefly  involved  shall 
break  down.  Those  organ  systems  that  have  evolved 
farthest  away  from  original  primitive  conditions  are 
the  soundest  and  most  resistant,  and  wear  the  longest 
under  the  strain  of  functioning.  So  then,  tlie  second 
large  result  is  that  it  is  the  way  potentially  innnortal 
cells  are  put  together  in  mutually  dependent  organ  sys- 
tems that  immediately  determines  the  time  relations  of 
the  life  span. 

But  it  was  possible  to  penetrate  more  deeply  into  the 
problem  than  this  by  finding  that  the  duration  of  life  is 
an  inherited  character  of  an  indi\idual,  passed  on  from 
parent  to  otfspring,  just  as  is  eye  color  or  hair  color,  and 
with  a  relatively  liigii  degree  of  precision.  Tliis  has 
been  proved  in  a  variety  of  ways,  first  directly  for  man 
(Pearson)  and  for  a  lower  animal,  Drosophila,  (Hyde, 
Pearl)  by  measuring  the  degree  of  hereditary  transmis- 
sion of  duration  of  life,  and  indirectly  by  showing  that 
the  death  rate  was  selective  (Pearson,  Snow,  Bell,  Ploetz) 
and  had  been,  since  nearly  the  beginning  of  recorded  his- 
tory, at  least.  It  is  heredity  wliich  determines  the  way 
the  organism  is  put  together — the  organization  of  the 
parts.  And  it  is  when  parts  break  down  and  tlie  organ- 
ization is  upset  that  death  comes.  So  the  third  large  re- 
sult is  that  heredity  is  the  primary  and  fundamental 
determiner  of  the  length  of  the  span  of  life. 

Finally,  it  is  possible  to  say  probably,  though  not  as 
yet  definitely  because  the  necessary  mass  of  experimen- 
tal evidence  is  still  lacking,  but  will,  I  believe,  be  shortly 
provided,  that  environmental  circumstances  play  their 

15 


226  BIOLOGY  OF  DEATH 

part  ill  determining  the  duration  of  life  largely,  if  not 
in  principle  entirely,  by  influencing  the  rate  at  which  the 
vital  patrimony  is  spent.  If  we  live  rapidly,  like  Loeb 
and  Northrop 's  Drosophila  at  the  high  temperatures,  our 
lives  may  be  more  interesting,  but  they  will  not  be  so 
long.  The  fact  appears  to  be,  though  reservation  of 
final  judgment  is  necessary  till  more  returns  are  in, 
that  heredity  determines  the  amount  of  capital  placed  in 
the  vital  bank  upon  which  we  draw  to  continue  life,  and 
which  when  all  used  up  spells  death ;  wliile  environment, 
using  the  term  in  the  broadest  sense  to  include  habits 
of  life  as  well  as  physical  surroundings,  determines  the 
rate  at  which  drafts  are  presented  and  cashed.  The 
case  seems  in  principle  like  what  obtains  in  respect  of  the 
duration  of  life  of  a  man-constructed  macliine.  It  is 
self-evident  that  if,  of  two  automobiles  of  the  same  make 
leaving  the  factory  together  new  at  the  same  time,  one  is 
run  at  the  rate  of  1,000  miles  per  year  and  the  other  at 
the  rate  of  10,000  miles  per  year,  the  useful  life  of  the 
former  is  bound  to  be  much  longer  in  time  that  that  of 
the  latter,  accidents  being  excluded  in  both  cases.  Again, 
a  very  high  priced  car,  well-built  of  the  finest  material, 
may  have  a  shorter  duration  of  life  than  the  poorest 
and  cheapest  machine,  pro\dded  the  annual  mileage  output 
of  the  former  is  many  times  that  of  the  latter. 

The  first  three  of  these  conclusions  seem  to  be  firmly 
grounded.  The  last  rests,  at  present,  upon  a  less  secure 
footing.  Because  it  does,  it  offers  an  extremely  promis- 
ing field  for  both  statistical  and  experimental  research. 
We  need  a  wide  variety  of  investigations,  like  those  of 
Loeb  and  Northrop,  of  Slonaker  and  of  Kubner,  on  the 
experimental  side.     On  the  statistical  side,  well-conceived 


NATURAL  DEATH,  PUBLIC  HEALTH        227 

and  careful  studies,  by  the  most  refined  of  modern  meth- 
ods, upon  occupational  mortality  seem  likuly  to  yield 
large  returns. 

PUBLIC    HEALTH    ACTIVITIES 

Fortunately,  it  is  possible  to  get  some  ligkt  on  tlic 
environmental  side  from  existing  statistical  data  by  con- 
sidering, in  a  broad  general  way,  the  results  of  public 
health  activities.  Any  public  health  work,  of  course, 
deals,  and  can  deal  in  the  present  state  of  public  senti- 
ment and  enlightenment,  only  with  environmental  matters. 
Attempts  at  social  control  of  the  germ-plasm — the  innate 
inherited  constitutional  make-up — of  a  people,  by  eugenic 
legislation,  have  not  been  conspicuously  successful.  And 
there  is  a  good  deal  of  doubt,  having  regard  to  all  factors 
necessarily  involved,  whether  they  have  always  been 
even  well-conceived.  As  an  animal  breeder  of  some 
years'  experience,  I  have  no  doubt  whatever  that  almost 
any  breeder  of  average  intelligence,  if  given  omnipotent 
control  over  the  activities  of  human  beings,  could,  in  a 
few  generations,  breed  a  race  of  men  on  the  average  con- 
siderably superior — by  our  present  standards — to  any 
race  of  men  now  existing  in  respect  of  many  qualities  or 
attributes.  But,  as  a  practical  person,  I  am  equally  sure 
that  nothing  of  the  sort  is  going  to  be  done  by  legislative 
action  or  any  similar  delegation  of  powers.  Before  any 
sensible  person  or  society  is  going  to  entrust  the  control 
of  its  germ-plasm  to  politics  or  to  science,  there  will  be 
demanded  that  science  know  a  great  deal  more  than  it 
now  does  about  the  vagaries  of  germ-plasms  and  how  to 
control  them.  Another  essential  diniculty  is  one  of  stan- 
dards.    Suppose  it  to  be  granted  that  our  knowledge  of 


228  BIOLOGY  OF  DEATH 

genetics  was  sufficiently  ample  and  profound  to  make  it 
possible  to  make  a  racial  germ-plasm  exactly  whatever 
one  pleased;  what  individual  or  group  of  individuals 
could  possibly  be  trusted  to  decide  what  it  should  be? 
Doubtless  many  persons  of  uplifting  tendencies  would 
promptly  come  forward  prepared  to  undertake  such  a 
responsibility.  But  what  of  history?  If  it  teaches  us 
anything,  it  is  that  social,  moral  and  political  standards 
are  not  fixed  and  absolute,  but  vary,  and  vary  radically 
in  both  space  and  time.  And  further,  history  teaches 
that  a  great  many  of  the  most  valuable  people,  in  the 
highest  and  best  sense,  whom  the  world  has  ever  kno^vn, 
were  so  constituted  physically,  morally';  or  otherwise, 
as  to  make  it  certain  that  under  a  strict  eugenic  regime 
they  never  would  have  existed  at  all.  One  cannot  but 
feel  that  man's  instinctive  wariness  about  experimental 
interferences  with  his  germ-plasm  is  in  considerable 
degree,  well-founded. 

But  because  of  the  altogether  more  impersonal  na- 
ture of  the  case,  most  men  individually  and  society  in 
general  are  perfectly  willing  to  let  anybody  do  anything 
they  like  in  the  direction  of  modifying  the  environment  in 
what  is  believed,  or  hoped  to  be,  the  direction  of  improve- 
ment, or  trying  to,  quite  regardless  of  whether  science 
is  able  to  give  any  slightest  inkling  on  the  basis  of  ascer- 
tained facts  as  to  whether  the  outcome  mil  be  good,  bad 
or  indifferent.  Hence  many  kinds  of  weird  acti^dties  and 
propaganda  flourish  like  the  proverbial  bay  tree. 

Of  all  organized  activities  looking  towards  the  direct 
modification  of  the  environment  to  the  benefit  of  mankind, 
that  group  comprised  under  the  terms  sanitation,  hygiene 


NATURAL  DEATH,  PUBLIC  HEALTH    229 

and  public  health  have,  by  all  odds,  the  best  case  when 
measured  in  terms  of  accomplishment.  Man's  expecta- 
tion of  life  has  increased  as  he  has  come  down  through 
the  centuries  {cf,  Pearson  and  ^Macdonell.)  A  large 
part  of  tliis  improvement  must  surely  be  credited  to  his 
improved  understanding  of  how  to  cope  with  an  always 
more  or  less  inimical  environment  and  assuage  its  asper- 
ities to  his  greater  comfort  and  well-being.  To  fail  to 
give  this  credit  w^ould  be  manifestly  absurd. 

But  it  would  be  equally  absurd  to  attempt  to  main- 
tain that  all  decline  in  the  death-rate  which  has  occurred 
has  been  due  to  the  efforts  of  health  officials,  w^hether 
conscious  or  unconscious,  as  is  often  asserted  and  still 
more  often  implied  in  the  impassioned  outpourings  of 
zealous  propagandists.  The  open-minded  student  of  the 
natural  history  of  disease  knows  perfectly  well  that  a 
large  part  of  the  improvement  in  the  rate  of  mortality 
cannot  possibly  have  been  due  to  any  such  efforts.  To 
illustrate  the  point,  I  have  prepared  a  series  of  illustra- 
tions dealing  mth  conditions  in  the  Registration  Area 
of  the  United  States  in  the  immediate  past.  All  these 
diagrams  (Figures  52,  53,  and  54)  give  death-rates  per 
100,000  from  various  causes  of  death  in  the  period  of 
1900-1918,  inclusive,  both  sexes  for  simplicity  being  taken 
together.  The  lines  are  all  plotted  on  a  logarithmic 
scale.  The  result  of  this  method  of  plotting  is  that  the 
slope  trend  of  each  line  is  directly  comparable  with  that 
of  any  other,  no  matter  what  the  absolute  magnitude  of 
the  rates  concerned.  It  is  these  slopes,  measuring  im- 
provement in  mortality,  to  which  T  would  especially 
direct  attention. 


230  BIOLOGY  OF  DEATH 

CONTROLLABLE.      CAUSES     OF  DEATH 


IfiOO  r^ 


100 


§ 

o 

§ 


1^ 

5 


;3: 


0.1 


Zi^^S^^^ffSfS    or     rH€    LUNGS 


\. — . — ^^ 


^^^ 


I  I  I  I  I  I  I  I  I  I  I  I  I  I  I  I  I 


1900  01    OZ  03  04  05  Ob  07  Od  09  10   II    l^    /J    lA    i5  16   17  Id 

YEAR 


Fig.  52. — Trend  of  death  rates  for  four  causes  of  death  against  which  public  health  activities 

have  been  particularly  directed. 

In  figure  52  are  given  the  trends  of  the  death-rates 
for  four  diseases  against  wliich  pnblic  health  and  sani- 
tary activities  have  been  particularly  and  vigorously 


I 


NATURAL  DEATH,  PUBLIC  HEALTH        231 

directed,  with,  as  we  are  accustomed  to  say,  most  grati- 
fying results.     The  diseases  are: 

1.  Tuberculosis   of   the   lungs. 

2.  Typhoid  fever. 

3.  Diphtheria    and    croup. 

4.  Dysentery. 

We  note  at  once  that  the  death-rates  from  these 
diseases  have  all  steadily  declined  in  tlio  19  years  under 
review.  But  the  rate  of  drop  lias  been  sli^^litly  uncfiual. 
Remembering  that  the  slopes  are  comj)arable,  where- 
ever  the  lines  may  lie,  and  that  an  equal  slope  means  a 
relatively  equally  effective  diminution  of  the  mortality 
of  the  disease,  we  note  that  the  death-rate  from  tuber- 
culosis of  the  lungs  has  decreased  slightly  less  than  any 
of  the  other  three.  Yet  it  may  fairly  be  said  that  so 
strenuous  a  warfare,  or  one  engaging  in  its  ranks  so  many 
earnest  and  active  workers,  has  probably  never  in  the 
history  of  the  world  been  waged  against  any  disease  as 
that  which  has  been  fought  in  the  Ignited  States  against 
tuberculosis  in  the  period  covered.  The  rates  of  decline 
of  the  other  three  diseases  are  all  practically  identical. 

Figure  53  shows  entirely  similar  trends  for  four 
other  causes  of  death — namely: 

1.  Bronchitis    (acute  and  chronic). 

2.  Paralysis  without  specified  cause. 

3.  Purulent  infection  and  septicaemia. 

4.  Softening  of  the  brain. 

Now  it  will  be  granted  at  once,  I  think,  that  public 
health  and  sanitation  can  have  had,  at  liie  utmost,  ex- 
tremely little,  if  anything,  to  do  with  the  trend  of  mor- 
tality from  these  four  causes  of  death.  For  the  most 
part  they  certainly  represent  j)atli()l(>gical  entities  far 
beyond  the  present  reach  of  the  health  ulUcer.     Yet  the 


232 

1,000 


BIOLOGY  OF  DEATH 

NON  -  CONTROLLED     CAUSES     OF  DEATH 


100 


o 
o 

o 


0.    10 


5 


f 
§ 


0.1 


'--"^"^Zi^w. 


'^/q 


anaf    CA 


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S. 


I      I      I      I      I      I      I      I 


1900  01    02  03  04  05  06   07  03   09  10    II     II    13    I4-    15    16    17    Id 

YEAR 


Fio.  53. — Trend  of  death  rates  from  four  causes  of  death  upon  which  no  direct  attempt  at 

control  has  been  made. 

outstanding  fact  is  that  their  rates  of  mortality  have  de- 
clined and  are  declining  just  as  did  those  in  the  control- 
lable group  showTi  in  Figure  52.     It  is  of  no  moment 


NATURAL  DEATH,  PUBLIC  HEALTH        233 


1.000 


100 


o 


q:  10 


d..£2^^0u^SLC 


^^L/S€S 


"••»"••• 


5 


^ 

^ 


0.1 


^^os. 


'^es 


IQOO  01  0^  03  04-  05  06  07  08  09  10    II    IZ    13    i-i-    /J    16    I7   id 

YEAR 


FiQ.  54. — Trend  of  combined  death  rate  from  the  four  causes  shown  in  Figure  52  as  compart 

with  the  four  causes  shown  in  Figure  53. 

to  say  that  the  four  causes  of  death  in  the  second  group 
are  absolutely  of  less  importance  than  some  of  those  in 
the  first  group,  because  what  we  are  here  discussing 
is  not  relative  force  of  mortality  from  dilferent  causes, 


234  BIOLOGY  OF  DEATH 

but  rather  the  trend  of  mortality  from  particular  causes. 
The  rate  of  decline  is  just  as  significant,  whatever  the 
absolute  point  from  which  the  curve  starts. 

It  is  difiicult  to  carry  in  the  mind  an  exact  impression 
of  the  slope  of  a  line,  so,  in  order  that  a  comparison  may 
be  made,  I  have  plotted  in  Figure  54,  first,  the  total  rate 
of  mortality  from  the  four  controllable  causes  of  death 
taken  together  and,  second,  the  total  rate  of  mortality 
from  the  four  uncontrolled  causes  taken  together.  The 
result  is  interesting.  The  two  lines  were  actually  nearer 
together  in  1900  than  they  were  in  1918.  They  have 
diverged  because  the  recorded  mortality  from  the  uncon- 
trolled four  has  actually  decreased  faster  in  the  19  years 
than  has  that  from  the  four  against  which  we  have  been 
actively  fighting.  The  divergence  is  not  great,  however. 
Perhaps  we  are  only  justified  in  saying  that  the  mortality 
in  each  of  the  two  groups  has  notably  declined,  and  at  not 
far  from  identical  rates. 

Now  the  four  diseases  in  tliis  group,  T  chose  quite  at 
random  from  among  the  causes  of  death  whose  rates  I 
knew  to  be  declining,  to  use  as  an  illustration  solely.  I 
could  easily  pick  out  eight  other  causes  of  death  which 
would  illustrate  the  same  point.  I  do  not  ^\ish  too  much 
stress  to  be  laid  upon  these  examples.  If  they  may  serve 
merely  to  drive  sharply  home  into  the  mind  that  it  is  only 
the  tyro  or  the  reckless  propagandist,  long  ago  a  stranger 
to  truth,  who  mil  venture  to  assert  that  a  declining  death- 
rate  in  and  of  itself  marks  the  successful  result  of  human 
effort,  I  shall  be  abundantly  satisfied. 

It  has  been  objected  that  the  decline  shown  by  the 
four  ^^non-controlled''  causes  in  the  example  just  dealt 
with  is  due  w^holly,  or  nearly  so,  to  changes  in  the  practice 
of  physicians  relative  to  the  reporting  of  the  cause  of 


NATURAL  DEATH,  PUBLIC  HEALTH        235 

death,  and  that,  therefore,  the  decline  is  spurious.  I  have 
not  been  able  to  find  that  there  is  any  good  evidence  that 
this  is  the  fact;  that,  in  short,  changes  in  reporting  prac- 
tice have  affected  the  ** non-controlled"  group  more  than 
the  ** controllable"  group.  But  another  kind  of  exain]jle 
may  be  cited  to  illustrate  the  same  general  point.  Suppose 
we  compare  the  course  of  mortality  from  certain  wull- 
delined  causes,  about  the  reporting  of  which  there  can  be 
no  controversy,  in  (a)  a  group  of  countries  standing  in  an 
advanced  position  in  matters  of  public  health,  sanitation, 
etc.,  and  (b)  a  group  of  countries  relatively  backward  and 
undeveloped  in  these  respects.  Such  a  comparison  is  im- 
possible to  make  over  any  long  period  of  time  because  of 
lack  of  comparable  data.  I  have  succeeded  in  getting  com- 
parable statistics  on  two  diseases,  namely  typhoid  fever 
and  diphtheria,  for  the  period  1898  to  1912  inclusive,  for 
the  following  countries : 

A.     Countries     having     (in    period      B.     Countries     having     (in     period 

covered)       highly  developed                  covered)  less  highly  developed 

public  health  and  sanitation.  public  health   and   sanitation 

Australia  than  those  in  group  A. 

Austria  Italy 

England  and  Wales  Jamaica 

Germany  Kouniania 

Without  going  into  detailed  comi)arisons,  which  might 
be  thought  invidious,  it  is  evident  on  the  face  of  the  case, 
I  think,  that  the  countries  in  the  A  group  w(»re,  on  the 
average  during  the  period  covered,  much  more  advanced 
in  all  practical  public  health  matters  than  were  the  coun- 
tries in  group  B. 

In  Figures  55  and  56  are  shown  the  trends  of  the 
weighted  average  death  rates  from  typhoid  fever  and 
diphtheria  respectively  in  the  two  groups  of  countries. 

It  is  e\ddent  from  these  diagrams  that  the  death  rates 


236 


BIOLOGY  OF  DEATH 


from  these  two  causes  declined,  during  the  period  cov- 
ered, in  both  the  A  and  the  B  groups  of  countries  and 
at  not  far  from  the  same  rate.  There  is  no  such  large 
difference  as  would  be  expected  if  organized  human  inter- 
ference mth  the  natural  history  of  disease  always  played 


100 


"yi 


10 


TYPHOID      FLVER 


- -.ff^^^ 


••-    ♦. 


••». •• 


'•^^OOA 


1698    99    1900    01      0^     03     04     05     06      O?     08     09 

YEAR 


10       II       1^ 


Fio.  55. — Course  of  the  weighted  average  death  rate,  for  the  countries  in  the  A  (solid  line) 

and  B  (broken  line)  groups,  from  typhoid  fever. 

the  role  of  immediate  and  large  importance  which  the 
propagandist  asserts  that  it  does. 

To  guard  against  the  possibility  of  any  misunder- 
standing, let  me  say  quite  specifically  and  categorically, 
that  the  above  is  not  intended  in  any  way  to  convey  the 
idea  that  public  health  work  is  not  desirable,  or  that  a 


NATURAL  DEATH,  PUBLIC  HEALTH        237 

laissez-faire  policy  would  be  better,  or  that  public  health 
efforts  have  not  been  enormously  valuable  in  connection 
with  typhoid  fever  and  diphtheria.  My  purpose  is  quite 
other,  being  solely  a  desire  to  emphasize  two  things,  viz: 
1.  That  the  trend  of  human  mortalitv  in  time  is  an 


18^    39    000    01 


03     04      05      06 
YEAR 


07     06     OO      10 


II 


|^ 


Fia.  56. — Like  figure  55,  but  for  diphtheria  and  croup. 

extraordinarily  complex  biological  phenomenon,  in 
wliich  many  factors  besides  the  best  efforts  of  hoiillh 
officials  are  involved. 

2.  That  for  manv  causes  of  death  a  vast  lot  needs  to 
be  added  to  our  knowledge  of  etiolog}',  in  the  broadest 
sense,  before  really  efficient  control  can  Ik'  ho]^ed  for. 
This  knowledge  can  come  only  through  scientiiic  investi- 


238  BIOLOGY  OF  DEATH 

gation,  and  not  through  the  complacent  acceptance  of  the 
propagandist's  assurance  that  ^^if  what  knowledge  we 
now  have  is  applied,  all  will  be  well.''* 

Many  others  have,  of  course,  perceived  that,  in  the 
natural  history  of  disease,  mortality  from  particular 
causes  may  decline  over  long  periods  of  time  without  any 
relation  to  what  health  departments  have  done,  or  tried 
to  do  about  it.  For  example,  Given  has  recently  pointed 
out  that  there  is  no  evidence  that  anything  that  man  has 
done  has  affected,  in  either  one  way  or  the  other,  the 
decline  in  the  mortality  of  tuberculosis,  which  has  been 
continuous  for  nearly  three-quarters  of  a  century. 
Pearson  has  discussed  the  same  point. 

There  is  much  in  our  public  health  work  that  is  worthy 
of  the  highest  praise.  When  based  upon  a  sound  founda- 
tion of  ascertained  fact  it  may,  and  does,  proceed  with  a 
step  as  firm  and  inexorable  as  that  of  Fate  itself,  to  the 
wiping  out  of  preventable  mortality.  Two  recent  ex- 
amples may  be  cited  here,  by  way  of  specific  illustration 
of  what  real  and  reasonably  complete  scientific  knowledge 
can  accomplish  in  public  health  work.  Both  examples 
are  taken  from  the  work  of  the  International  Health 
Joard  of  the  Rockefeller  Foundation,  with  the  permission 
of  its  director,  Mr.  Wickliffe  Rose. 

The  first  concerns  malaria.  The  life  cycle  of  the 
malaria  parasite  is  definitely  kno\\ai,  and  furnished  a 


*  One  can  but  wonder  if  the  many  scientific  men,  who  permit,  and  to 
some  extent  approve,  such  assertions,  have  ever  thought  of  the  menace  to 
the  continued  support  of  research  in  science  in  general  which  inheres  in 
this  attitude  of  mind.  The  support  of  research  comes  finally  back  always 
to  society  in  general — to  the  "average  citizen"  in  short.  Is  it  the  part 
of  wisdom  to  leave  his  education  as  to  the  meaning  and  significance  of 
science  for  his  happiness  and  well-being,  so  entirely  in  the  hands  of  the 
propagandist  as  we  now  do?     Has  anti-vivisection  taught  no  lesson? 


NATURAL  DEATH,  PUBLIC  HEALTH   239 

definite  scientific  basis  for  control  procedure.  *'lt  is 
well  understood,  not  only  by  scientists,  but  also  by  intel- 
ligent laymen,  that  the  spread  of  the  infection  may  b(; 
prevented  by  mosquito  control,  by  protectin^^  people  I'roni 
being  bitten  by  mosquitoes,  or  by  destroying  the  parasite 
in  the  blood  of  the  human  carrier.  It  has  been  sIkjwu, 
moreover,  by  repeated  demonstrations,  that  by  applica- 
tion of  any  one  of  these  measures,  or  of  any  combination 
of  them,  the  amount  of  malaria  in  a  community  may  Ix* 
reduced  indefinitely.  There  are  few  diseases  that  pre- 
sent so  many  vulnerable  points  of  attack  and  none  j^er- 
haps  the  control  of  which  may  be  made  more  definite 
or  certain/'  (Rose). 

In  1916  the  International  Health  Board  undertook 
some  experiments  in  control  at  Crossett,  Ark.  In  des- 
cribing the  work  Rose  says: 

"Effort  has  been  made  to  test  the  feasibility  of  malaria  control  ii» 
small  communities  by  resort  to  such  simple  anti-moscjnito  measure  as 
would  fall  within  the  limits  of  expenditure  that  such  communities  mi},'ht 
well  afford.  The  habits  of  the  three  mosquitoes — .1.  (piadrimaruUitus  Say. 
A.  punctipennis  Say,  and  A.  cruzians  Wiodermann — which  are  ropunsihle 
for  the  infection  in  these  communities  have  been  made  the  subject  of 
constant  study  with  a  view  to  eliniinutiii;^  all  unnecessary  effort,  and  tluTi'by 
reducing  coat. 

"Experiment  at  Crossett,  11)16 — The  first  of  tlit'se  tests  was  undertaken 
at  Crossett,  a  lumber  town  of  2,129  inhabitants,  situated  in  Ashley  County 
in  south-eastern  Arkansas,  about  12  miles  north  of  the  Louisiana  line 
Crossett  lies  at  the  edge  of  the  so-called  "uplands,"  in  a  level,  low-lying 
region  (elevation  165  feet),  with  sufficient  undulation  to  provide  reason- 
ably good  natural  drainage.  Climatic  conditions  and  aljundant  breeiling 
places  favor  the  propagation  of  anopheles.  Malaria,  in  its  severe  form, 
is  widely  prevalent  as  an  endemic  infection,  and  according  to  the  estimate 
of  local  physicians,  is  the  causo  of  about  GO  per  cent,  of  all  illness  through- 
out the  region.  Within  the  town  itself  the  nmlaria  rale  was  high,  and 
was  recognized  by  the  lumber  corporation  and  the  people  as  a  seriou* 
menace  to  health  and  working  ellieicncy. 

"The  initial  step  in  the  experiment  was  a  survey  of  the  community 
to  determine  the  malaria  incidence,  to  ascertain  in  the  species  of  niosquitoeti 


240  BIOLOGY[OF  DEATH 

responsible  for  the  spread  of  the  infection,  and  to  locate  the  breeding  places 
of  these  mosquitoes.  Breeding  places  were  exhibited  on  a  community 
map,  and  organized  effort  was  centered  on  their  destruction  or  control. 
The  program  of  simple  measures  excluded  all  major  drainage.  Barrow 
pits  and  shallow  ponds  were  filled  or  drained;  streams  were  cleared  of 
undergrowth  when  necessary  to  let  the  sunlight  in;  their  margins  and  beds 
were  cleared  of  vegetation  and  obstruction;  and  they  were  trained  to  a 
narrow  channel,  thus  providing  an  unobstructed  off-flow.  Artificial  ^con- 
tainers were  removed  from  premises ;  water  barrels  on  bridges  were  treated 
with  nitre  cake.  All  remaining  breeding  places  were  regularly  treated  by 
removing  vegetation,  opening  up  shallow  margins  to  give  free  access  to 
small  fish,  and  spraying  once  a  week  with  road  oil  by  means  of  automatic 
drips  or  a  knapsack  sprayer.  All  operations  were  under  the  supervision 
of  a  trained  lay  inspector.  Care  was  exercised  to  eliminate  all  unnecessary 
effort  and  to  secure,  not  the  elimination  of  the  last  mosquito,  but  a  rea- 
sonably high  degree  of  control  at  a  minimum  cost." 

The  results  are  sliowu  in  Figure  57,  as  measured  by 
a  number  of  physicians'  calls  for  the  treatment  of  ma- 
laria in  the  community. 

The  second  examijle  shows  the  effectiveness  of  con- 
trol of  yellow  fever,  another  disease  for  which  definite 
scientific  knowledge  exists  as  to  etiology  and  mode 
of  transmission. 

Nothing  could  more  convincingly  demonstrate  than 
does  Figure  58  the  effectiveness  ^^dth  wliich  this  disease 
can  be  controlled.  The  diagram  shows  the  results  of 
the  International  Health  Board's  yellow  fever  work  in 
Guayaquil  in  1918-1920. 

t 

THE  POPULATION   PROBLEM 

Turning  to  another  phase  of  the  problem,  it  is  appar- 
ent that  if,  as  a  result  of  sanitary  and  hygienic  activi- 
ties and  natural  evolution,  the  average  duration  of 
human  life  is  greater  now  than  it  used  to  be  and  is  getting 
greater  all  the  time,  then  clearly  there  must  be  more 
people  on  the  earth  at  any  time,  out  of  a  given  number 


NATURAL  DEATH,  PUBLIC  HEALTH        241 


Malaria  Control  at 

CROSSETT-ARKAr 

SSA5 

Calls    for  Malaria 

191 

5                      1916                     1917 

1918 

SBO 

S60 

sto 

S2o 

40O 

46C 

:^:: 

420 

;    L           .6s     

400 

._         ____JL__X 

380 

1               QJ 

■  !        ^ 
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1  i           b^                         _        __ 

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L-I t 

Z-—1L 

i  _is t_ 

Z        I 

1   Tli^* 

Mini  i  1 

1  1  1  III  1  n  1  iiiiiiiiiiiii 

i  n  1 II n ni nniiiiiiiiiii 

«^  HH  ■  ■  ■  ■  1 

[iTiinrrTiTni    t^  m. 

"  " 

Miii'iM    1  iiippnmmi 

ill   .._-_..-.  T 

lilil] 

1 

:          ^  1 

Monthly 

Distribution  of  Calls                  Popula 

tion,  2029 

'5 

"^          '^/6          1^1       m     TotslOalts 

1^15            2500 

JAN                A 
FEB                A 
MAKCH            i 
APRIL                ( 
MAY                  i 

^5            40               C             3 

^5             39                7             2 
>G            59              13            4 
>0             81                12              8 
)0             1(4               31              2 

/9/6   '-         741 
/917     -         200 
/?'«     -         71 

JUNE               1 

20             98                13             «        ^jy^Z^'^S^ 

Reductton, 

iV5-i^i6           97. » 

JUL/                2i 
AU^                3 
SEPT               5< 
OCT                 W( 
MOT.                3 

acs.  .     .     1( 

00              'y^                  ^                0 

50            91               33             7       Per  Capita  C 

X)              54               22               II 

30             46                14              8 

50              2D               a3              7 

30               4                 15             10 

\0St: 

191^     -            124 

/9/7     -             *3 
/y/9     -             -53 

FiQ.  57. — Record  of  malaria  control  by  anti-mosquito  measures,  CroMott.  Ark.   1916-1918. 

(From  Rose). 

16 


242 


BIOLOGY  OF  DEATH 


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-Disappearance  of  yellow  fever  from  Guayaquil.  Ecuador,  as  a  result  of  control 
measures.  (By  permission  of  International  Health  Board). 


NATURAL  DEATH,  PUBLIC  IILAL'ni        213 

born,  than  was  formerly  the  case.  It  is  fiirlhcrnirire 
plain  tliat  if  nothinii:  liappens  to  tlio  l»irl}i-rat('  I  hero  must 
eventually  be  as  many  persons  livinic  upon  the  hal)ital»le 
parts  of  the  g-lo])c  as  can  possibly  be  supported  with 
food  and  the  other  necessities  of  life.  Malthus,  whom 
every  one  discusses  but  few  take  the  trou])le  to  read, 
pointed  out  many  years  ago  that  the  prol>Iom  of  ])opu- 
lation  transcends,  in  its  direct  importance  to  the  welfare 
of  human  beings  and  forms  of  social  organization,  all 
other  problems.  Lately  we  have  had  a  demonstration  on 
a  ghastly  gigantic  scale  of  the  truth  of  Malthus*  conten- 
tion. For,  in  last  analysis,  it  cannot  be  doubted  that  one 
important  underlying  cause  of  the  great  war,  through 
which  we  have  just  passed,  was  the  ever-growing  pres- 
sure of  population  upon  subsistence. 

Any  system  or  form  of  activity  which  tends,  by  how- 
ever slight  an  amount,  to  keep  more  people  alive  at  a  given 
instant  of  time  than  would  otherAvdse  remain  alive,  adds 
to  the  difficulty  of  the  problem  of  population.  We  have 
just  seen  that  tliis  is  precisely  what  our  public-health 
activities  aim  to  do,  and  in  which  they  succeed  in  a  not 
inconsiderable  degree.  But  someone  will  say  at  once 
that,  while  it  is  true  that  the  death-rate  is  falling  more 
or  less  generally,  still  the  birth-rate  is  falling  concomi- 
tantly, so  we  need  not  worry  about  the  population  prob- 
lem. It  is  evident  that  if  we  regard  the  population 
problem  in  terms  of  world-area,  rather  than  that  of  any 
particular  country,  its  degree  of  immediacy  depends  upon 
the  ratio  of  births  to  deaths  in  any  given  time  unit.  If 
we  examine,  as  T  have  recently  done,  these  death-liirth 
ratios  for  different  countries,  we  (in<l  Ihat  tliey  give  us 
little  hope  of  any  solution  of  the  problem  of  population 


244 


BIOLOGY  OF  DEATH 


by  virtue  of  a  supposed  general  positive  correlation  be- 
tween birth-rates  and  death-rates. 

The  relation  of  birth-rate  and  death-rate  changes  to 
population  changes  is  a  simple  one  and  may  be  put  this 
way.  If,  neglecting  migration  as  we  are  justified  in 
doing  in  the  war  period  and  in  considering  the  world  prob- 
lem, in  a  given  time  unit  the  percentage 

100  Deaths 
Births 

has  a  value  less  than  100,  it  means  that  the  births  exceed 
the  deaths  and  that  the  population  is  increasing  within 
the  specified  time  unit.  If,  on  the  other  hand,  the  per- 
centage is  greater  than  100,  it  means  that  the  deaths  are 
more  frequent  than  the  births  and  that  the  population 
is  decreasing,  again  mthin  the  specified  time  unit.     The 

TABLE  29 

Percentage  of  Deaths  to  Births 


Year 

77  non-invaded 

departments 

of  France 

Prussia 

Bavaria 

England  and 
Wales 

1913 

97  per  cent. 
110  per  cent. 
169  per  cent. 
193  per  cent. 
179  per  cent. 
198  per  cent. 
154  per  cent. 

58  per^cent. 

74  per  cent. 

98jper  cent. 
131  per  cent. 
127  per  cent. 
146  per  cent. 

57  per  cent. 

1914 
1915 
1916 
1917 
1918 
1919 

66  per  cent. 
101  per  cent. 
117  per  cent. 
140  per  cent. 
132*  per  cent. 

59  per  cent. 
69  per  cent. 
65  per  cent. 
75  per  cent. 
92  per  cent. 
73  per  cent. 

1920 

42*  per  cent. 

*  First  three-fourths  of  yeax  only. 


ratio  of  deaths  to  births  may  be  conveniently  designated 
as  the  vital  index  of  a  population. 

From  the  raw  data  of  births  and  deaths,  I  have  cal- 
culated the  percentage  which  the  deaths  were  of  the  births 
for  (a)  the  77  non-invaded  departments  of  France;  (b) 


NATURAL  DEATH,  PUBLIC  HEALTH        245 

Prussia;  (c)  Bavaria;  and  (d)  England  and  Wales,  from 

1913  to  1920  by  years.     The  results  are  shown  in  Table  29. 

The  points  to  be  especially  noted  in  Table  29  are: 

1.  In  all  the  countries  here  dealt  with  the  death-]>lrth 
ratio  in  general  rose  throughout  the  war  ])eriod.  This 
means  that  the  proportion  of  deaths  to  births  increased 
so  long  as  the  war  continued. 

2.  But  in  England  it  never  rose  to  the  100  per  cent, 
mark.  In  other  words,  in  spite  of  all  the  dreadful  effects 
of  war,  England's  population  went  on  making  a  not 
increase  throughout  the  war. 

3.  Immediately  after  the  war  was  over,  the  death- 
birth  ratio  began  to  drop  rapidly  in  all  countries.  In 
England  in  1919  it  had  dropped  back  from  the  high  figure 
of  92  per  cent,  in  1918  to  73  per  cent.  In  France  it  dropped 
from  the  high  figure  of  198  in  1918  to  154  in  1919,  a 
lower  figure  than  France  had  sho^vn  since  1914.  In  all 
the  countries  the  same  change  is  occurring  at  a  rapid  pace. 

Perhaps  the  most  striking  possible  illustration  of  this 
is  the  history  of  the  death-birth  ratio  of  the  city  of 
Vienna,  showai  in  Figure  4,  with  data  from  the  United 
States  and  England  and  Wales  for  comparison.  Prob- 
ably no  single  large  city  in  the  w^orld  was  so  hard  hit  by 
the  war  as  Vienna.  Yet  observe  what  has  hai)pened  to 
its  death-birth  ratio.  Note  how  sharp  is  the  decline  in 
1919  after  the  peak  in  1918.  In  other  words,  we  see 
how  promptly  the  growth  of  population  tends  to  regulate 
itself  back  tow^ards  the  normal  after  even  so  disturbing 
an  npset  as  a  great  war. 

In  the  United  States,  the  death-birth  ratio  was  not 
affected  at  all  by  the  war,  though  it  was  markedly  altered 
by  the  influenza  epidemic.  The  facts  are  shown  in  Fig- 
ure 59  for  the  only  years  for  wdiich  data  are  available. 


246 


BIOLOGY  OF  DEATH 


The  area  covered  is  the  United  States  birth  registration 
area.  We  see  that  with  the  very  low  death-birth  ratio 
of  56  in  1915,  there  was  no  significant  change  till  the 
influenza  year  1918,  when  the  ratio  rose  to  73  per  cent. 


'S50 


GIZ 


J9I3  '  "    1914.     '       i9lS  I9l0  1917  l^ig  i&'&  '^^O 


WEAR 


Fig.  59. — Showing  the  change  in  percentage  which  deaths  were  of  births  in  each  of  the 

years  1912  to  1919  for  Vienna  ( ');  1915  to  1919  for  the  United  States  ( );  and 

1912  to  1920  for  England  and  Wales( ). 

But  in  1919,  it  promptly  dropped  back  to  the  normal  value 
of  57.98,  almost  identical  with  the  1917  figure  of  57.34. 

In  England  and  Wales,  the  provisional  fig-ure  indi- 
cates that  1920  will  show  a  lower  value  for  the  vital 
index  than  that  country  has  had  for  many  years. 

So  we  see  that  neither  a  highly  destructive  war,  nor 
the  most  destructive  epidemic  since  the  Middle  Ages, 
serves  more  than  to  cause  a  momentary  hesitation  in  the 
steady  onward  march  of  population  growth. 


NATURAL  DEATH,  PUBLIC  IILALTII        1>17 

The  first  thing  obviously  needed  in  any  scientific 
approach  to  the  problem  of  popnlation  is  a  j^'oixt  mathe- 
matical determination  and  expression  of  the  law  of  popu- 
lation growth.  It  has  been  seen  that  the  most  devastating 
calamities  make  but  a  momentary  flicker  in  the  steady 
progress  of  the  curve.  Furthermore,  ])()pulation  j^rowth 
is  plainly  a  biological  matter.  Tt  depends  upon,  in  last 
analysis,  only  the  basic  biological  phenomena  of  fertility 
and  mortality.  To  the  problem  of  an  adequate  mathe- 
matical expression  of  the  normal  growth  of  ])oj)ulations, 
my  colleague,  Dr.  Lowell  J.  Reed,  and  T  have  addressed 
ourselves  for  some  time  past.  The  known  data  upon  which 
we  have  to  operate  are  the  population  counts  given  by 
successive  censuses.  Various  attempts  have  been  made 
in  the  past  to  get  a  mathematical  representation  of  these 
in  order  to  predict  successfully  future  populations,  and 
to  get  estimates  of  the  population  in  inter-censal  years. 
A  noteworthy  attempt  of  this  sort  is  Pritchett's  fitting 
of  a  parabola  of  the  third  order  to  the  United  States  popu- 
lation from  1790  to  1880  inclusive.  Tliis  gave  a  fairly 
good  result  over  the  period,  Init  was  obWously  ])urely 
empirical,  expressed  no  real  biological  law  of  change, 
and  in  fact  failed  badly  in  prediction  after  1890. 

We  have  approached  the  problem  from  an  a  priori 
basis,  set  up  a  hj'pothesis  as  to  the  more  ini])<)rtant 
biological  factors  involved,  and  tested  the  resulting 
equation  against  the  facts  for  a  variety  of  countries. 
The    hypothesis    was    built    up    around    the    foll()^\^ng 

considerations : 

1.  Li  any  given  land  area  of  fixiMJ  limits,  as  Ity 
political  or  natural  boundaries,  there  nuist  necessarily  be 
an  upper  limit  to  the  number  of  persons  tliat  can  be  sup- 
ported on  the  area.     To  take  an  extreme  case,  it  is  obvious 


248  BIOLOGY  OF  DEATH 

that  not  so  many  as  25,000  persons  could  possibly  stand 
upon  an  acre  of  ground,  let  alone  live  on  it.  So,  similarly, 
there  must  be  for  any  area  an  upper  limiting  number  of 
persons  who  can  possibly  live  upon  it.  In  mathematical 
terms  this  means  that  the  population  curve  must  have 
an  upper  limiting  asymptote. 

2.  At  some  time  in  the  more  or  less  remote  past  the 
population  of  human  beings  upon  any  given  land  area 
must  have  been  nearly  or  quite  zero.  So  the  curve  must 
have  somewhere  a  lower  limiting  asymptote. 

3.  Between  these  two  levels  we  assume  that  the  rate 
of  growth  of  the  population,  that  is,  the  increase  in 
numbers  in  any  given  time  unit,  is  proportional  to  two 
things,  namely: 

a.  The  absolute  amount  of  growth    (or  size  of  population)    already 

attained ; 

b.  The  amount  of  as  yet  unutilized,  or  reserve,  means  or  sources  of 

subsistence    still    available    in    the    area    to    support    further 
population. 

These  hypotheses  lead  directly  to  a  curve  of  the  form 
shown  in  Figure  60,  in  which  the  position  of  the  asymp- 
totes and  of  the  point  of  inflection,  when  the  population 
is  growing  at  the  most  rapid  rate,  are  shown  in  terms 
of  the  constants.  It  is  seen  that  the  whole  history  of  a 
population,  as  pictured  by  this  curve,  is  something  like 
this:  In  the  early  years  following  the  settlement  of  a 
country  the  population  growth  is  slow.  Presently  it 
begins  to  grow  faster.  After  it  passes  the  point  where 
half  the  available  resources  of  subsistence  have  been 
drawn  upon  and  utilized,  the  rate  of  growth  becomes 
slower,  until  finally  the  maximum  population  which  the 
area  will  support  is  reached. 


NATURAL  DEATH,  PUBLIC  HEALTH        249 

This  theory*"  of  population  growth  makes  it  possible 
to  predict  what  the  maximum  popuhition  in  a  ^iven  area 
will  be,  and  when  it  wdll  be  attained.  Furthermore,  one 
can  tell  exactly  when  the  population  is  growing  at  the 
maximum  rate.     To  test  the  theor}%  we  have  only  to  fit 


Fia.  60. — Showing  a  theoretical  curve  of  population  growth. 

this  theoretical  curve  to  the  kno^\Tl  facts  of  population 
for  any  country  by  appropriate  mathematical  methods. 
If  the  hypothesis  fits  w^ell  all  the  known  facts  for  a  variety 
of  countries  in  different  stages  of  population  growth,  it 
may  w^ell  be  regarded  as  a  first  approximation  to  a  sub- 
stantially correct  hypothesis  and  expressive  of  tlie  bio- 
logical law  according  to  wdiich  population  grows.  In 
making  this  test  the  statistician  has  somewhat  the  same 

*  The  mathematical  hypothesis  here  dealt  with  is  essentially  the  wime 
as  that  of  Verhulst,  put  forth  in  1844.  As  Pearl  and  Keod  pointc<l  out 
in  their  first  paper  on  the  hubjcct  it  is  a  special  ease  of  a  much  more 
general  law.  A  eomj)reliensive  general  treatment  of  tlie  prolilem  we  are 
publishing  shortly  in  another  place.  The  generalization  in  no  way  alt€r8 
the  conclusions  drawn  here  from  a  few  illustrative  examples. 


250 


BIOLOGY  OF  DEATH 


kind  of  problem  that  confronts  the  astronomer  calculat- 
ing the  complete  orbit  of  a  comet.  The  astronomer  never 
has  more  than  a  relatively  few  observations  of  the  posi- 


19^274- 
175 


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UNITED    STATES 


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nOO    20    40     60    80    1600  20     40     60     80     I900  20     40     60     60    £000  £0    40     60     SO    £100 

YEARS 

Fig.  61. — Showing  the  curve  of  growth  of  the  population  of  the  United  States.     For  further 
explanation  of  this  and  the  two  following  diagrams,  see  text. 

tion  of  the  comet.  He  has,  from  Newtonian  principles, 
a  general  mathematical  expression  of  the  laws  of  motion 
of  heavenly  bodies.  He  must  then  construct  his  whole 
curve  from  the  data  given  by  the  few  observations.  So, 
similarly,  the  statistician  has  but  a  relatively  few  popu- 
lation observations  because  census  taking  has  been  prac- 
tised along  present  lines  only  a  little  more  than  a  century. 
According  to  the  stage  in  historical  development  of  the 
country  dealt  with,  he  may  have  given  an  early,  a  late,  or 
a  middle  short  piece  of  the  population  ** orbit''  or  his- 
tory. From  this  he  must  construct,  on  the  basis  of  his 
general  theory  of  ** population  orbits,''  the  whole  history, 
past  and  future,  of  the  population  in  question. 

To  demonstrate  how  successful  the  population  curve 
shoAvn  in  Figure  60  is  in  doing  this,  three  diagrams  are 
presented,  each  illustrating  the  growth  of  the  population 


NATURAL  DEATH,  PUBLIC  HEALTH   2ol 

ill  a  different  country.  Tlio  lioavy  solid  jjortion  of  each 
curve  shows  the  region  for  wliich  census  data  exist.  The 
lighter  broken  part  of  the  curve  shows  the  portioiiii  out- 
side this  observed  range.  The  circles  show  the  actual, 
kno\\Ti  observations.     The  first  curve  deals  with  the  popu- 


AI360 


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5;    ^s 


FRANCE 


% 


20 


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4 


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t600   ZO     4-0      60    60    rrOO  ZO    *0     to     eo     JdOO  ZO     40     60     eo     OOO  ZO     40      to     so    ZOOC 

Y€AJ?S 
Fig.  62. — Showing  the  curve  of  growth  of  the  population  of  France. 

lation  of  the  United  States.  Here  the  observations  come 
from  the  first  part  of  the  curve,  when  tlu^  popiihiti<ni  was 
leaving  the  lower  asymptote.  First  should  be  noted  thi' 
extraordinary  accuracy  with  which  the  niathomatical 
theory  describes  the  kno^\^l  facts.  It  would  be  extremely 
difficult,  by  any  process,  to  draw  a  curve  tlirt)ugh  the  ob- 
served circles  and  come  nearer  to  hitting  them  all  than 
this  one  does. 

Before  considering  the  detailed  consequences  of  this 
United  States  curve  in  relation  to  the  whoh*  popiihition 
history  of  the  country,  let  us  lirst  examine  some  curves 
for  other  countries,  where  the  observed  data  ft'll  in  (luite 
different  portions  of  the  ^'population  orbit."     Figure  iVl 


252  BIOLOGY  OF  DEATH 

gives  the  curve  for  France.  Since  before  the  time  when 
definite  census  records  began,  France  has  been  a  rather 
densely  populated  country.  All  the  data  mth  which  we 
had  to  work,  belong  therefore,  towards  the  final  end  of 
the  whole  population  history  curve.  The  known  popula- 
tion data  for  France  and  for  the  United  States  stand  at 
opposite  ends  of  the  whole  historical  curve.  One  is  an 
old  country  whose  population  is  nearing  the  upper  limit; 
the  other  a  new  country  whose  population  started  from 
near  the  lower  asymptote  only  about  a  century  and  a  half 
ago.  But  it  is  seen  from  the  diagram  that  the  general 
theory  of  population  growth  fits  perfectly  the  known  facts 
regarding  France's  population  in  the  120  years  for  which 
records  exist.  While  there  are  some  irregularities  in  the 
observation,  due  principally  to  the  effects  of  the  Franco- 
Prussian  war,  it  is  plain  that  on  the  whole  it  would  be 
practically  impossible  to  get  a  better  fitting  line  through 
the  observational  circles  than  the  present  one. 

We  have  seen  that  the  general  theory  of  population 
describes  with  equal  accuracy  the  rate  of  growth  in  a 
young  country,  vdih  rapidly  increasing  population,  and 
an  old  country,  where  the  population  is  approaching  close 
to  the  absolute  saturation  point.  Let  us  now  see  how  it 
works  for  a  country  in  an  intermediate  position  in  respect 
of  population.  Figure  63  shows  the  population  history 
of  Serbia.  Here  it  will  be  noted  at  once  that  the  heavy 
line,  which  denotes  the  region  of  knoAvn  census  data,  lies 
about  in  the  middle  of  the  whole  curve.  Again  the  fit 
of  theory  to  observation  is  extraordinarily  close.  No 
better  fit,  by  a  general  law  involving  no  more  than  3  con- 
stants, could  possibly  be  hoped  for. 

I  think  that  these  three  examples,  which  could  be 
multiplied  to  include  practically  every  country  for  which 


NATURAL  DEATH,  PUBLIC  HEALTH    253 

accurate  population  data  exist,  furnish  a  cogent  demon- 
stration of  the  essential  soundness  and  accuracy  of  this 
theory  of  population  growth.  Indeed,  the  facts  warrant, 
I  believe,  our  regarding  this  as  a  first  approximation  to 
the  true  natural  law  of  poi)nlati()n  ^n-owth.     AVe  now  are 


4.388 


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rrOO   20     ^'    60    60    wo  ZO     ao     60    eO    boo  20    40     60     eo    2000  20    40     CO     eo    2jOO 

YEARS 
Fig.  63. — Showing  the  curve  of  growth  of  the  population  of  Serbia. 

approaching  the  proper  mathematical  foundation  on 
which  to  build  sociological  discussions  of  the  problem 
of  population. 

As  a  further  demonstration  of  the  soundness  of  this 
theory  of  population  growth,  let  attention  be  directed  for 
a  moment  to  an  example  of  its  experimental  verification. 
To  a  fruit  fly  (Drosophila)  in  a  half  pint  milk  bottle,  such 
as  is  used  in  experimental  work  on  these  organisms,  the 
interior  of  the  bottle  represents  a  definitely  limited  uni- 
verse. How  does  the  fly  population  gi'ow  in  such  a  uni- 
verse? We  start  a  bottle  with  a  male  and  female  lly, 
and  a  small  sample,  say  10,  of  their  offs])ring  of  dilTerent 
ages  (larva?  and  pupa*).     The  results  are  shown  in  Fig- 


254 


BIOLOGY  OF  DEATH 


ure  64.  The  circles  give  the  observed  population  growth, 
obtained  by  census  counts  at  3-day  intervals.  There  can 
be  no  doubt  that  this  population  has  grown  in  accordance 
with  the  equation.  The  two  final  observations  lie  below 
the  curve,  because  of  the  difficulty  experienced,  in  this 


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Th    or   DR030PHILA 

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P 

POPULATION 

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Fig.  64. — Showing  the  growth  of  a  DrosophUa  population  kept  under  controlled 

experimental  conditions. 

particular  experiment,  of  keeping  the  food  supply  in  good 
condition  after  so  long  a  period  from  the  start. 

Let  us  return  to  the  further  discussion  of  the  popu- 
lation problem  of  the  United  States  in  the  light  of 
the  curve. 

The  first  question  which  interests  one  is  this:  When 
did  or  will  the  population  curve  of  this  country  pass  the 
point  of  inflection  and  exhibit  a  progressively  diminishing 
instead  of  increasing  rate  of  growth!  It  is  easily  deter- 
mined that  this  point  occurred  about  April  1,  1914,  on  the 
assumption  that  our  present  numerical  values  reliably  rep- 
resent the  rate  of  population  growth  in  this  country. 
In  other  words,  so  far  as  we  may  rely  upon  present  nu- 
merical values,  the  United  States  has  already  passed  its 
period  of  most  rapid  population  growth,  unless  there 


1 


NATURAL  DEATH,  PUBLIC  HEALTH        255 

comes  into  play  some  factor  not  now  known,  and  which 
has  never  operated  during  the  T)ast  liistorv  of  the  oountrv 
to  make  the  rate  of  growth  more  rapid.  'Hir  latter  con- 
tingency appears  impro])a])le.  The  l!):i()  census  confirms 
the  result,  indicated  ])y  the  curve,  that  the  period  of  most 
rapid  population  growth  was  passed  somewhere  in  the 
last  decade.  The  population  at  the  point  of  intlcction 
works  out  to  have  been  98,G37,00(),  which  was,  in  fact, 
about  the  population  of  the  country  in  LJ14. 

The  upper  asymptote  given  by  the  equation  has  the 
value  of  197,274,000  roughly.  This  means  that  tlie  ma.\i- 
mum  population  which  continental  United  States,  as  now 
areally  limited,  w^ill  have,  wdll  be  roughly  twice  the  pres- 
ent population;  provided  no  fundamental  new  factor 
comes  into  play  in  the  meantime,  different  in  its  magni- 
tude and  mode  of  operation  from  any  of  the  factors  which 
have  influenced  population  growth  in  the  past.  This 
state  of  affairs  will  be  reached  in  about  the  year  2,11)0,  a 
little  less  than  two  centuries  hence.  Perhaps  it  may  be 
thought  that  the  magnitude  of  this  number  is  not  sufti- 
ciently  imposing.  It  is  so  easy,  and  most  writers  on 
population  have  been  so  prone,  to  extrapolate  population 
by  geometric  series  or  by  a  parabola  or  some  such  purely 
empirical  curve,  and  arrive  at  stupendous  figun^s,  that 
calm  consideration  of  real  probabilities  is  most  dillicult 
to  obtain.  Wliile  ^VQ  regard  the  numerical  results  as 
only  a  rough  first  approximation,  it  remains  a  fact  that 
if  anyone  will  soberly  think  of  every  city,  every  village, 
every  to\vm  in  tliis  country  having  its  present  population 
multiplied  by  2,  and  will  further  think  of  twice  as  many 
persons  on  the  land  in  agricultural  pursuits,  he  will  be 
bound,  we  think,  to  conclude  that  the  country  would  be 


256  BIOLOGY  OF  DEATH 

fairly  densely  populated.     It  would  have  about  66  per- 
sons per  square  mile  of  land  area. 

It  will  at  once  be  pointed  out  that  many  European 
countries  have  a  much  greater  density  of  population  than 
66  persons  to  the  square  mile,  as,  for  example,  Belgium 
with  673,  the  Netherlands  with  499,  etc.  But  it  must  not 
be  forgotten  that  these  countries  are  far  from  self- 
supporting  in  respect  of  physical  means  of  subsistence. 
They  are,  or  were  before  the  war,  economically  self- 
supporting,  which  is  a  very  different  thing,  because,  by 
their  industrial  development  at  home  and  in  their  colo- 
nies, they  produce  money  enough  to  buy  physical  means 
of  subsistence  from  less  densely  populated  portions  of 
the  world.  We  can,  of  course,  do  the  same  thing,  pro- 
vided that  by  the  time  our  population  gets  so  dense  as  to 
make  it  necessary,  there  still  remain  portions  of  the  globe 
where  food,  clothing  material  and  fuel  are  produced  in 
excess  of  the  needs  of  their  home  populations. 

Now  197,000,000  people  mil  require,  on  the  basis  of 
our  present  food  habits,  about  260,000,000  million  calories 
per  annum.  The  United  States,  during  the  seven  years 
1911-1918,  produced  as  an  annual  average,  in  the  form  of 
human  food,  both  primary  and  secondary  (i.e,,  broadly 
vegetable  and  animal),  only  137,163,606  million  calories 
per  year.  So  that,  unless  our  food  habits  radically  change, 
and  a  man  is  able  to  do  with  less  than  3,000  to  3,500  calories 
per  day,  or  unless  our  agricultural  production  radically 
increases,  which  it  appears  not  likely  to  do  for  a  variety 
of  reasons  which  cannot  be  here  gone  into,  it  will  be 
necessary,  when  even  our  modest  figure  for  the  asymptotic 
population  is  reached,  to  import  nearly  or  quite  one-half 
of  the  calories  necessary  for  that  population.  It  seems 
improbable  that  the  population  will  go  on  increasing  at 


NATURAL  DEATH,  PUHIJC  1I]:ai;HI        257 

any  very  rapid  rate  after  such  a  eoiiditiuii  is  reached. 
East  has  shown  that  the  United  States  has  alremlv  entered 
upon  the  era  of  dimiuisliint!:  returns  in  agriculture  in  this 
country.  Is  it  at  all  reasonable  to  suj)pose  that  hy  the  time 
this  country  has  closely  a])])roache(l  the  asymptote  here 
indicated,  with  ail  the  competition  lOr  means  of  suIh 
sistence  which  the  already  densely  ])o])ulated  countries  of 
Fjurope  will  then  ])e  puttinii:  up,  there  can  he  found  any 
portion  of  the  i»'l()])0  producin<i:  food  in  excess  of  its  own 
needs  to  an  extent  to  make  it  possible  for  us  to  find  the 
calories  we  shall  need  to  imi)ort? 

Altogether  we  believe  it  ^^^ll  be  the  part  of  wisdom 
for  anyone  dis])osed  to  criticize  our  asym])totic  value  of 
a  hundred  and  ninety-seven  and  a  quarter  millions  ])ecause 
it  is  thought  too  small,  to  look  further  into  all  the  rele- 
vant facts.  This  point  of  view  is  sustained  in  a  recent 
paper  by  East  in  which  the  future  agricultural  resources 
of  the  country  are  particularly  examined. 

The  relation  of  this  already  pressing  problem  of  popu- 
lation to  the  problem  of  the  duration  of  life  is  obvious 
enough.  For  every  point  that  the  death  rate  is  lowered 
(or,  what  is  the  same  thing,  the  average  duration  of  life 
increased)  the  prol)lem  of  po]iulation  is  made  more  imme- 
diate and  more  difficult  unless  there  is  a  correspcuiding 
decrease  in  the  birth-rate.  Is  it  to  be  wondered  at  that 
most  thougbtful  students  of  the  problem  of  population 
are  advocates  of  birth  control?  Or  Is  it  r.-marknble 
that  Major  Leomird  Darwin,  president  of  the  Kugenics 
Education  Society  in  Hngland,  should  say  in  a  carefully 
considered  memorandum  to  the  new  British  Ministry  of 
flealth:  *^In  the  interests  of  posterity  it  is  most  desirable 
that  parents  should  now  limit  the  size  of  their  families 
by  any  means  held  by  them  to  be  right   (provided  such 

17 


258  BIOLOGY  OF  DEATH 

means  are  not  injurious  to  health,  nor,  like  abortion,  an 
otfense  against  public  morals)  to  such  an  extent  that  the 
children  could  be  brought  up  as  efficient  citizens  and  mth- 
out  deterioration  in  the  standards  of  their  civilization; 
and  that  parents  should  not  limit  the  size  of  the  family 
for  any  other  reasons  except  on  account  of  definite  hered- 
itary defects,  or  to  secure  an  adequate  interval  between 
births." 

I  am  able  to  make  no  prediction  as  to  how  civilized 
countries  will  solve  (if  they  do  solve)  the  problems 
arising  out  of  the  impending  saturation  with  human  popu- 
lation of  the  portion  of  the  earth's  surface  habitable  by 
man.  The  certainty  and  assurance  with  wliich  various 
ones  of  my  friends  advance  solutions  excites  my  wonder 
and  admiration.  But  what  impresses  me  even  more 
is  that  scarcely  any  two  of  them  agree  on  the  nature 
of  the  panacea.  To  some  it  is  birth  control,  to  others 
svnthetic  foods  derived  from  the  atmosphere  or  else- 
where,  and  so  on. 

For  mvself ,  I  am  content  if  I  have  succeeded,  in  even 
a  small  measure,  in  indicating  that  population  growth  pre- 
sents a  problem  fast  becoming  urgent;  a  problem  that 
in  its  overwhelming  signiificance  and  almost  infinite  rami- 
fications touches  upon  virtually  every  present  human  ac- 
tivity and  interest,  and  in  particular  upon  the  acti\dties 
comprised  in  the  terms  public  health  and  hygiene. 


Library 
N,   C.   State    College 


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INDEX 


Acaiiihias,  3S 

Accidental  deutlis,  lUT 

Activity,  mctiihulic,  211-217 

Agamic  reproduction,  33,  35,  37,  41, 
77 

Alchemy,  19 

Alimentary  tract,  107,  108,  110,  112, 
129-131 

Amicronucleate  races,  72,  73 

Amma,  K.,  39,  259 

Amphibia,  longevity  of,  22 

Analysis  of  life  tables,  94-101 

Animals,  longevity  of,  22,  G8 

Anopheles  cruzians,  239 

punctipennis,  239 
quadrimaculatus,  239 

Anti-vivisection,  238 

Apple  trees,  37,  74,  75 

Artificial  parthenogenesis,  51-58,  223 

Ascaris,  39 

Aseptic  life,  43,  200-202 

Astrology,  19 

Australia,  235 

Austria,  235 

Autogamy,  73 
Automobiles,  220 

Bacteria,  rOle  of,  in  duration  of  lift', 

43,  199-202 
Bataillon,  52,  259 
Bavaria,  244,  245 
Bee,  senility  in,  28 
Beeton,  M.,  166,  169,  171,  2.VJ 
Belgium,  256 
Bell,  A.  G.,   152-158,   165,   166,  225, 

259 
Benedict,  H.  N.,  44,  259 
Bertillon,  J.,  216,  259 


Bibliography,  259-288 

Bills  of  mortality,  79 

Biological  classificatiun  of  cauMs  of 

death,   101-137 
Birds,  longevity  of,  22,  63 
Birth  control,  257 

injuries  at,    121,    123 
premature,  121,  123 
Blood,  107,   108.   111.   lis.   11«> 
Body  size  and  longevity,  26,  68 

■weight.  OS 
Bogdanow,  K.  A.,  200,  259 
Brain  ^veight,  68 
Brazil,   106 
Brighfs  disease,   161 
Bronchitis,  231,  232 
Brown,  J.  \V.,  206,  261 
Brownlee,  J.,  183 
Budding,  37 
Bulloch,  W.,  259 
Burrows,  M.  T.,  59-62,  260 

Callithrix,  68 

Calories,  256 

Cancer  cells,  61 

Carrel,  A.,   10,  61-65,   73,  74,   76-78, 

224,  260 
Cat,  61 

Cattell,  J.  McK.,   10 
Causes  of  death,   102-137 

bioli>gical    dassili- 

catii»n  of.   104 
international  clas- 
sifuation  of,  103 
non-controlled, 
232,  233 
Cells,  interstitial.  219 
Cellular   immortality,  51-78 

269 


270 


INDEX 


Centenarians,  23-26,  64 

Cephalic  index,  175 

Cephalisation,  68 

Chances  of  death,  79-101 

Changes  in  expectation  of  life,  82-94 

Chick,  59-61,  76 

duration  of  life  of,  63 
Child,  C.  M.,  34-36,  39,  43,  44,  260 
Child  welfare,  112 
Chironomus,  39 
Circulatory   system,    107,    108,    111, 

118,  119 
Classification,   biological,   of   causes 

of  death,  104 
international,  of 
causes  of  death,  103 
Clocks,  analogy  with  living  things, 

150,  151,  198 
Clonal  reproduction,  37,  74 
Coefficient  of  correlation,  168 
Coelenterates,  62 
Cohnheim,  J.,  44,  260 
Collis,  E.  L.,  216,  260 
Conjugation,  30-33,  71,  73 
Conklin,  E.  G.,  29,  44,  260 
Controllable  causes  of  death,  230,  233 
Correlation  coefficient,   168 
Correlations  in  duration  of  life,  168- 

177 
Crossett,  239,  241 
Croup,  230,  231 
Crum,  F.  S.,  184,  260 
Culture  of  tissues  in  vitro,  58-78 
Curve,  mortality,  graduation  of,  94- 
101 
specific  death  rate,  114,   116 
Curves,  logarithmic  plotting  of,  114 
Cyclops,  39 
Cytomorphosis,  28 
Cytoplasm,  29,  44 

Darwin,  L.,  257 
Davis,  W.  H.,  113 
Dawson,  J.  A.,  73,  260 


Dawson,  M.  M.,  82,  260 
Death,  appearance  of  in  evolution,  42 
biological     classification     of 

causes  of,  104-137 
chances  of,  79-101 
causes  of,  102-137 
the  Marksman,  96-98 
theories  of,  43-50 
Death  birth  ratio,  243-246 
Death-rate,  selective,  177-185 
Death-rates,  crude,  112 

specific,  112-137 
DeDecker,  A.,  216,  267 
Deer,  68 

Delage,  Y.,  45,  260 
Delcourt,  A.,  200,  260 
Descent,  method  of,  40-42 
Diarrhoea,  110,  112 
Differentiation,  45-47,  67,  75 
Diphtheria,  230,  231,  235,  237 
Diseases,  preventability  of,  162 
Doflein,  F.,  33,  260 
Dog  fish,  39 

Domestic  fowl,  duration  of  life  of,  63 
Donaldson,  H.  H.,  29,  260 
Drosophila    mclanogaster,     186-202, 
208-211,  214,  222,  225,  226,  253, 
254 
Dublin,  L.   I.,  82,   113,  260,  261 
du  Xoiiy,  P.  L.,  77 
Duration  of  life,  correlation  in,  168- 

177 
experimental  study 

of,  186-222 
influence  of  activi- 
ty on,  211-217 
influence    of    tem- 
perature on,  208- 
217 
inheritance  of,  94, 

160-185 
in  man,  79-94,  150- 
185 


INDEX 


271 


Duration  of  life  of  domestic  fowl,  G.J 

of  pareiit*i  and  olT- 

Kpriii^',   !">')- 157 
rOle  of  bacteria  in, 

43,   199-202 
variation  in,  21,  22, 
08,  80-82 
Dysentery,  230,  231 

East,  E.  M.,  ID."),  2.')7,  201 

Ebeling,  A.  H.,  60,  01,  74,  70,  77,  78, 

260,  261 
Ectoderm,  138-149 
Effects  of  public  health  work,   112, 

227-242 
Egypt,  expectation  of  life  in,  87-89 
Elephant,  longevity  of,  22 
Embryology  and  mortality,  138-149 
Embryonic  juice,  74 
Endocrinal    system,    107,    108,    112, 

133,    134 
Endoderm,   138-149 
Endomixis,  30,  33,  71-73 
Energy,  213-217 
England,  106,  108-111,  139,  140,  235, 

244-246 
Enriques,  P.,  73,  261 
Environment,  225,  226 
Epidemic,  influenza,  245 
Erdman,  R.,  30,  201,  268 
Eudorina  elegans,  31,  73 
Eugenics,  227 

Education  Society,  257 
Evolutionary  progress  in  longevity, 

87-94 
Evolution  of  ectoderm,    141 
of  endodtrin,   141 
of  mesoderm,   141 
of  workmanship  of,   148 
Excretory  organs,  107,  108,  111,  120, 

127 
Exercise,  212,  213 
Expectation  of  life,  defined.  82 

changes  in,  82-94 


i-xpecttttion  of  life,  effect  of  itelertion 

on,  94 
hyjH»thptiral,  164 
in  ant-ient  E^pt, 

87-80 
in  ancieut  Home, 

90  92 
ill   Hihipania  and 
Lubitania,    91- 
92 
i  n       K  o  til  a  n 
Africa,  92  93 
Experimental   study   of  duration   of 

life,  180-222 
Eye  color,  174,  175 

Fermat,  82 

Fertilizin,  57 

Fish,  longevity  of,  22 

Fisher,  A.,  101,  149,  184,  261 

Fisher,  I.,  161,  162,  165 

Fission,  32,  33,  35,  40,  41 

Fitting  the  mortality  curve,  94- 101 

Food  recjuirements,  256 

Forsyth,   C.   H.,   161,    104,  261 

Fowl,  duration  of  life  of,  63 

France,  244,  245,  251,  252 

Franco-Prussian  wur,  2.'»2 

Fraternal  correlations,  171.  172.  175, 

170 
Friedenthal,  H.,  68,  69,  261 
Friends'   Provident   association,    167 
Frog,  52,  58,  59 

Galvani,  58 

Genealogy  of  Hyde  family,   152 

Genetic  variation,    190 

Germany,  235 

Germ  cells,  37-42,  51-58 

layers,  138 

plasm,  227,  228 
Given.  I).  H.  C,  238,  201 
CJland,  pituitary,   220-222 
Glands,  puberty.  217-219 


272 


INDEX 


Glaucoma  pyriformis,  73 

Glover,  J.  W.,  80,  84,  88,  90-92,  261 

Gonads,  217-219 

Gonococcus  infection,  123,  124 

Graduation  of  mortality  curve,  94- 

101 
Grafting,  37 
Graunt,  J.,  79 

Greenwood,  M.,  205,  216,  259-261 
Groth,  205,  261 

Growth    of    Drosophila    population, 
254 
of  populations,  247-258 
Growth   of   United   States,   250-252, 

254-257 
Guayaquil,  240,  242 
Guinea  pig,  61 
Guyenot,  E.,  200,  260,  261 
Guyer,  M.  F.,  52,  262 

Hahn,  205,  261 

Halley,  E.,  81,  82,  84,  262 

Harper,  M.,  39,  262 

Harrison,  R.  G.,  58-60,  63,  64,  224, 

262 
Hartman,  M.,  31,  73,  262 
Heart  muscle,  61 
Hegner,  R.  W.,  40,  262 
Henderson,  R.,  99,  262 
Heron,  D.,  206,  262 
Hersch,  L.,  202,  203,  205,  206,  208, 

262 
Hertwig,  R.,  44,  263 
Hispania  and  Lusitania,  expectation 

of  life  in,  91-92 
Hodge,  C.  F.,  27,  28,  263 
Holland,  184 
Homicide,   107 
Homoiotoxin,  64 
Howard,  W.  T.,  44,  263 
Hyde  family,  152-166 
Hyde,  R.  R.,  198,  225,  263 
Hygiene,  227 


Immortality,  cellular,  51-78 
human,  17-20 
of  protozoa,  30-33,  64 
of  somatic  cells,  58-78 
Industrial  mortalitv,  216 
Infant  mortality,  205,  206,  208 
Influence  of  activity  on  duration  of 
of  life,  211-217 
of   poverty    on   mortality, 

202-208 
of    serum    on    tissue    cul- 
tures, 76,  77 
of    temperature    on    dura- 
tion of  life,  208-217 
Influenza  epidemic,  245 
Inheritance  of  duration  of  life,  94 

in    Droso- 
phila, 
186-198 
in     m  a  n, 
150-185 
of    physical    characters, 
174,  175 
Injuries  at  birth,  121,  123 
Insects,  longevity  of,  22 
International  classification  of  causes 
of  death,  103 
Health      Board,     238- 
240,  242 
Interstitial  cells,  219 
Invertebrates,  longevity  of,  22 
In  vitro  culture  of  tissues,  58-78 
Italy,  235 

Jamaica,  235 

Jennings,  H.  S.,  31,  33,  40,  41,  45, 

71,  72,  263 
Jickeli,  C.  F.,  44,  263 
Jollos,  33,  263 
Jones,  D.  F.,  261 

Kassowitz,  M.,  44,  263 

Keimhahn,  40 

Kidneys,  61,  107,  108,  111,  126,  127 


INDKX 


273 


Kopf,  K.  W.,  ll.J.  JGO 
Korscliolt,  K.,  2G3 

Landed  Geiiliy,  1(»7.  !()'.>.   17-' 

Lankaster,  E.  K.,  2(>:\ 

Levassour,  E.,  S2.  203 

Le«;rand,  M.  A.,  2r):} 

Lewis,  ^L  Tv.,  02,  20;i 

Lewis,  W.  IL,  53,  54,  62,  263,  264 

Life,  aseptic,  43,  200-202 

ilian^^e.s  in  expectation  of,  82-lU 
curve  of  Hvde  family,    L")3 
cycle  of  Drosophila,  187,   188 
prolonp:in^,   17,  54,  218,  221 
table,  70-82 

analysis  of,  94-101 
Breslau,   83,   84,   02 
Carlisle,  83,  80 
U.   S.,   1010,  83-86 
Lillie,  F.  R.,  57,  263 
List,  International,  103 
Locomotor  ataxia,  124 
Loeb,  J.,  47,  52-55,  57,  200,  201,  208- 
211,  214,  215,  223,  220,  263,  264 
Loeb,  L.,  59,  64,  65,  67,  224,  264 
Logarithmic  plottin*^,   114 
London,  205-208 
Longevity,  body  size  and.  26 

evolutionary  progress  in, 

87-04 
of  animals,  22 
of  parents,   158,   160 
Lowell  Institute,  9,  27 

Macdonell.  \V.  R.,  87,  89-93,  229,  261 

Malaria,  238-241 

Malthus,  T.  K.,  243 

Mammals,  longevity  of,  22 

Man,  longevity  of,  23-26,  80-94 

Marmoset,  08 

Mendelian  inheritance,  194,  197,  108 

Mesoderm,  138-149 

Metabolic  activity,  211-217 

Metazoa,  31,  33,  40,  46.  71 


MetchnikofT.  E..  43,  109,  200,  264 

Methml  of  deftcent,  40-42 

MicronucleUH,  72 

Minot,  C.  8.,  27,  28,  44,  71.  264 

Mitchell.  P.  C,  264 

Mitosis,  fll 

M.)ntg(.m«Ty,  T.  II.,  44,  265 

Morgan,  T.  H.,   10,   iHrt.  197,  265 

Mortality,  billh  of,   79 

curve,  gruduntion  of,  04- 

101 
cmbrytdogical    1>a»is    of, 

138-149 
industrial,  216 
infant,  205,  206 
intliu'uce  of  poverty  on, 

2(t2-20S 
organ  system  in,  107,  lOS 

:Mo.s«iuito,  239.  240 

Most  fatal  organ  systems,  i;i6 

Mouse,  68,  220-222 

growth  of.   69  70 

.Miihlmann,  M.,  44,  265 

Muller,  J.,  44 

Miiller,  L.  R.,  265 

Muscular  system,  107,  108,  112,  127, 
128 

Xascher,  I.,  26,  27,  265 

Nerve  cells,  senile  clianges  in,  27-29 

Nervous  system,  107.  lOS.  130.   131 

Netherlands,  256 

Non-controlled  causes  of  death,  232. 

233 
Northrop,  J.   11..   200,  201,  209-211. 

214,  215,  226,  264,  265 
Nucleus,  29.  30,  44 

Occupation,  216 

Ogle.  W..  95 

Orbits,    250 

Oriran  systems  in  mortality,  107,  lOS 

most  fatal,   136 
Oxi/trichn  hiftnrnDStuma,  73 


274 


Paralysis,  231,  232 
Paramecium,  30-32,  35,  40,  72 
Parental  correlations,  171,  172,  174, 

176 
Parents  and  offspring,  duration  of 
life  of,  155-157 
longevity  of,   158,   160 
Paris,  202-206 
Parr,  T.,  24 

Parthenogenesis,  artificial,  51-58,  223 
Pascal,  82 

Pearl,  R.,  106,  201,  225,  249,  265 
Pearson,  K.,  19,  87-91,  93-101,  166, 
169-177,   179,   182,    183,   225,  229, 
238,  259,  266 
Peerage,  167,  169,  172 
Pennaria,  62 
Physical  characters,  inheritance  of, 

174,  175 
Pituitary  gland,  220-222 
Pixell-Goodrich,  Mrs.,  28 
Planaria  dorotocephala,  34,  35 
Plants,  senility  in,  44 
Ploetz,  A.,   178,   179,   182,   183,  225, 

266 
Population,  240-258 
Potassium  cyanide,  53,  54 
Poverty,  202-208 
Premature  birth,  121,  123 
Preventabilitv  of  diseases,   162 
Pritchett,  A.  S.,  247,  266 
Progress,  evolutionary,  in  longevity, 

87-94 
Prolonging  life,  17,  54,  218,  221 
Prostate,  126,  219 
Protozoa,  30-33,  40,  41,  46 

immortality  of,  30-33,  41, 
64,  71 
Prussia,  244,  245 
Puberty  glands,  217-219 
Public  health  work,  effects  of,  112, 

227-242 
Purulent  infection,  231,  232 


INDEX 

Quaker  records,  171,  173 


Rabbit,  68 

Rat,  61,  212,  213,  218 
Ratio,  death-birth,  243-246 
Ray,  L.  A.,  69,  70,  220,  221,  266 
Reed,  L.  J.,  247,  249,  266 
Registration  Area,  U.  S.,   106,   108, 
109,   139,   140,   164,  229,  245,  246 
Reproduction,  organic,   33,   41 
by  budding,  37 
by  fission,  32,  33,  41 
clonal,  37 
sexual,  37-40,  41 
Reptile,  longevity  of,  22 
Respiratory   system,    107,    108,    110, 

112,  119,  120,  136,  137 
Results,  summary  of,  223-227 
Richards,  H.  A.,  86,  87,  266 
Ritter,  W.  E.,  75,  266 
Robertson,  T.  B.,  69,  70,  220,  221,  266 
Rockefeller  Foundation,  238 
Institute,  52,  61 
Role  of  bacteria  in  duration  of  life, 

43,  199-202 
Roman   Africa,    expectation   of   life 

in,  92 
Rome,  expectation  of  life  in,  90-92 
Romeis,  B.,  219,  266 
Rose,  W.,  238,  239,  241,  266 
Roumania,  235 
Roundworm,  30 
Royal  families,  177 
Rubner,  M.,  213,  214,  226,  267 

Saleeby,  183 

Sanitation,  227,  235 

S5o  Paulo,  106,  108-111,  139,  140 

Sea  urchin,  52,  54,  57 

Selection,  effect  of,  on  expectation  of 

life,  94 
Selective  death  rate,  177-185 
Seneca,  102 


iM)i:x 


275 


Seneficonee,  27-.K).   4i».   70-7H 

theories  of.  4.*i  TiO 
Senile  clianjies   in   lu'ive  f«'lU,  "27  i'.l 
Senility  as  cause  of  deatli.    h)'.> 

in  plants.  44.  7  t.  7;') 
Septicipniiu,  231,  2:{2 
Serbia,  2r)2.  253 
Serum,    iiithioiice   on    ti>sMi'   cnllnrf. 

76.  77 
Sex   or«^aiis,    107,    lOS,    Ul.    12112... 

217-219 
Sexual  reproduction,  M  4\ 
Shell.  .]..  26,  27 
Skeletal  system,   1(»7,    Kts,    112.    127. 

128 
Skin,  107,  108,  110.  112,  131,  132 
Slonaker.  J.   M.,  212,  213,  218.  228. 

207 
Slotopolski.  B..  33.  267 
Snow,  E.  C,  179-183,  225,  267 
Softening  of  the  brain,  231.  232 
Soma,  40 

Somatic  cells,  immortality  of,  58  7 S 
Span,  174,  175 
Spiefxplltei-^.  W.,  87 
Spiritualism,   18-20 
Spleen,  61 
Spon«;es,  62 
Stature.  174,  175 
Steinach,  E.,  217-219,  267 
Stcnost07num,  35,  36 
Stevenson,  T.  H.  C,  206-208,  267 
Still  births,  205 
Strongylocentrotus    purpiinitiis.    .■).".. 

56 
Summary  of  results,  223-227 
Survivorship    lines    of    Drosophilu. 

188,  192.   195 
Syphilis,  123 


Table,  life.  79S2 

Temperature,  208-217 

Tethelin.  70.  220  222 

Thii)ries  of  deuth,  43  50 

Theory  of  population  );ruwtti.  J4'.i 

Thyroid  ^lUnxd,  01 

Tissue  culture  in   vitro,  5K  7K 
TranHplantation  of  tuinorit,  64,  tt.'> 
Iiibenulohih.  101,  204.  20^.  230   2.'tl 

238 
I  umor   traiii-plunlution,  04,  05 
Typhoid   fever,  2.30,  231,  235,  230 

I'nitetl    States,   jfrowth    of,   250  2.V2, 

254-257 
V  rusty  la  granfiin,  72 

Van  iiuren,  G.  ii..   113.  260 
N'ariation.  ^'enetic,   190 
X'enereal  diseases,    123,   124 
Verhulst.  P.  K..  249.  267 
\'erworn,  M.,  44.  207 
\ienna,  245.  246 
Voronoff,  217 

Waller,  A.   I).,  216.  267 

Walworth.   K.   II..    152.  207 

War,  243 

Wedekind.  33.  207 

Weismann,  A.,  20,  43.  65,  207 

Whale.  lon;.'evity  of,  22 

Wilson.  H.  v..  62,  267 

Wittstein.  99 

Womlruir.   L.   L..  30.  33.  72.  73.  267. 

208 
Wo(k1s.  F    a..  38.  39.  2r.S 

Vellnw    fever.   240.   242 
Y<.un''.  T.   K..  23  25.  208 


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